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98 publications mentioning rno-mir-133a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-133a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 202
Coincidently, while the expression level of snail 1 was obviously increased in the left ventricle of the infarcted heart at both 7 and 28 days post MI, miR-133 -overexpressing MSCs revealed more effective suppression of MI -induced snail expression than control-MSC or vector-MSC injection (Fig.   6f). [score:9]
We then searched for a potential direct mRNA target of miR-133 by a target prediction program, and identified two conserved miR-133 binding sites in the 3′UTR of the snail 1 gene (Fig.   6d). [score:6]
In this regard, two fibrosis-related genes Col1a1 and snail 1 were predicted targets of miR-133 by TargetScan (http://www. [score:5]
Further studies indicated that cardiac expression of snail 1 was significantly repressed by adjacent miR-133 -overexpressing MSCs, and both the inflammatory level and the infarct size decreased in miR-133-MSC -injected rat hearts. [score:5]
Consistently, our results indicated an increased expression of exosome biomarker CD63 in the miR-133 overexpression group. [score:5]
Besides, recent studies revealed the ability of miR-133, along with other transcription factors or miRNAs, to induce myocardial transdifferentiation of cardiac fibroblasts through inhibiting the expression of TGF-β signaling or factors which promote fibrosis, such as snail 1 [35, 36]. [score:5]
Our Q-PCR results further verified that overexpression of miR-133 in MSCs significantly repressed cardiac expression of the snail 1 gene. [score:5]
Transplantation of miR-133 -overexpressing MSCs provides an effective strategy for cardiac repair and modulation of cardiac-related diseases. [score:5]
These results suggested that miR-133 might enhance the survival of MSCs injected into the heart and influence the paracrine function of MSCs including miR-133 and other protein levels, and that miR-133 secreted from MSCs might suppress the expression of snail 1 in cardiomyocytes in vitro and in vivo and then influence the fibrosis of LV after MI. [score:5]
In this regard, miR-133 has been reported to be deregulated in human MI [18] and cardiac hypertrophy, while its overexpression was able to antagonize cardiac apoptosis [34] and protected the heart from ischemic injury in a mouse mo del of cardiac hypertrophy [23]. [score:4]
We undertook both overexpression and knockdown approaches to demonstrate the anti-apoptotic role of miR-133 on MSC survival and the cardioprotective role of miR-133-MSCs in infarcted hearts. [score:4]
Q-PCR revealed that transfection of miR-133 agomir elevated miR-133 expression in MSCs by 800-fold when compared with the negative control, and miR-133 antagomir reduced miR-133 expression by 80% (Fig.   1d). [score:4]
Regulatory exercise can prevent cardiac cell apoptosis through accelerating the expression of miR-133 and Bcl-2 [24]. [score:4]
PARP is a typical apoptosis related protein cleaved by caspase 3. We found that the full-length protein level of PARP was elevated in the miR-133 agomir group and downregulated in the miR-133 antagomir group (Fig.   2c), indicating that miR-133 decreased caspase 3 activity in MSCs. [score:4]
miR-133 enhances the survival of MSCs in vivo and reduces the cardiac expression of Snail 1 in vitro and in vivo. [score:3]
To study whether exosomes mediate the roles of miR-133-MSCs in the heart function after MI, the abundance of miR-133 was accessed in exosomes secreted by miR-133 -overexpressing or interfering MSCs. [score:3]
However, no change in cell viability and cell-cycle distribution was observed in control, miR-133 -overexpressed, and miR-133-interfered MSCs. [score:3]
However, cardiac expression of miR-133 significantly decreased in patients suffering from MI [18]. [score:3]
While sham-ligated rats were used as control, these rats under MI surgeries were divided into four groups receiving intramyocardial injection of PBS, normal MSCs, MSCs infected with empty lentivirus (vector-MSCs), or MSCs infected with miR-133 -overexpressed lentivirus (miR-133-MSCs), respectively. [score:3]
Correspondingly, we demonstrated in this study that miR-133 overexpression ameliorated inflammation and fibrosis in the infarcted heart. [score:3]
d miR-133 expression level detected by Q-PCR after lentiviral transfection of miR-133. [score:3]
d miR-133 expression level determined by Q-PCR. [score:3]
Previous data and our data illustrate that miR-133 could be an effective target to promote MSC survival in the ischemic myocardium microenvironment. [score:3]
The aim of this study was to elucidate the effects of miR-133 on the function of MSCs in treating ischemic myocardial diseases. [score:3]
A rat myocardial infarction mo del was created by ligating the left anterior descending coronary artery, while control MSCs (vector-MSCs) or miR-133 -overexpressed MSCs (miR-133-MSCs) were injected into the zone around the myocardial infarction. [score:3]
Xu C Lu Y Pan Z The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, HSP70 and caspase-9 in cardiomyocytesJ Cell Sci. [score:3]
For in-vivo studies, constitutive activation of miR-133 in MSCs was achieved by lentivirus -mediated miR-133 overexpression. [score:3]
What is more, miR-133 was reported to affect β-adrenergic receptor signaling and inhibit cardiac hypotrophy in the process of heart failure [22, 23]. [score:3]
miR-133 enhances the survival of MSCs in vivo and reduces the cardiac expression of Snail 1 in vitro and in vivoOne of the most important barriers to MSC therapy in MI is that many of the MSCs injected into the heart die in the hypoxic environment or are washed away with heart beating. [score:3]
Hypoxia -induced apoptosis of MSCs obviously reduced, along with enhanced expression of total poly ADP-ribose polymerase protein, after miR-133 agomir transfection, while the apoptosis rate increased in MSCs transfected with miR-133 antagomir. [score:3]
showed that, on the same amount, the exosome isolated from the miR-133 agomir group expressed a high level of CD63, a protein marker in the exosomes (Fig.   6c). [score:3]
The expression level of miR-133a was analyzed by quantitative RT-PCR (Q-PCR) using the miRNAs Quantitation Kit (GenePharma, China). [score:3]
Since the survival rate and activity are the two most important determinants of cell function, we assumed that miR-133 overexpression may improve the effect of MSCs on cardiac protection in the injured heart. [score:3]
In summary, this study demonstrated that miR-133 enhanced the therapeutic effect of MSCs in an acute MI mo del, by suppressing the apoptosis of MSCs under hypoxic conditions and mediating their paracrine effects. [score:3]
In this study, we revealed a protective function of miR-133 against hypoxia -induced MSC apoptosis, as well as more effectively improved cardiac function in the infarcted heart following transplantation of miR-133 -overexpressing MSCs. [score:3]
Zhang L Wu Y Li Y Tanshinone IIA improves miR-133 expression through MAPK ERK1/2 pathway in hypoxic cardiac myocytesCell Physiol Biochem. [score:3]
Subsequently, the expression level of miR-133a was analyzed by Q-PCR as already described. [score:3]
Habibi P Alihemmati A NourAzar A Expression of the Mir-133 and Bcl-2 could be affected by swimming training in the heart of ovariectomized ratsIran J Basic Med Sci. [score:2]
Bostjancic E Zidar N Stajer D MicroRNAs miR-1, miR-133a, miR-133b and miR-208 are dysregulated in human myocardial infarctionCardiology. [score:2]
Compared to the negative control, we further found a significant increase of the miR-133 level in exosomes secreted by miR-133 -overexpressing MSCs. [score:2]
By in-vitro coculture assay, we found that miR-133-MSCs significantly repressed the cardiac expression of snail 1 mRNA (Fig.   6e). [score:2]
Feng Y Niu LL Wei W A feedback circuit between miR-133 and the ERK1/2 pathway involving an exquisite mechanism for regulating myoblast proliferation and differentiationCell Death Dis. [score:2]
As shown in Fig.   3d, the miR-133 level was increased by 700-fold in MSCs infected by miR-133 -overexpressing lentivirus, when compared with that in both uninfected and vector-lentivirus-infected MSCs. [score:2]
At the same time, exosomes were isolated from the supernatant to analyze the paracrine miR-133. [score:1]
To evaluate the effect of miR-133 on cell survival in vivo, normal MSCs, MSCs infected with empty lentivirus (vector-MSCs), or miR-133 -overexpressed lentivirus (miR-133-MSCs) were dyed with chloromethylbenzamido (CellTracker [TM] CM-Dil 11372053; Invitrogen) according to the manufacturer’s instructions, followed by cell transplantation. [score:1]
Besides, LV mass and LV volume were also improved by miR-133-MSCs. [score:1]
Chen JF Man del EM Thomson JM The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiationNat Genet. [score:1]
We thus explored whether miR-133 could protect MSCs against apoptosis. [score:1]
At 7 and 28 days post MI, the LVEF and FS of infarcted rat hearts significantly decreased in the PBS group compared with the sham group, while both normal and miR-133 -overexpressing MSCs could partially rescue MI -induced decrease of LVEF and FS as shown in Fig.   4. More importantly, the LVEF was significantly increased in the miR-133-MSC group compared with the vector-MSC group (p < 0.05). [score:1]
We extracted the miR-133a and pre-miR133 sequences of rats in miRBase (http://www. [score:1]
miR-133 was recently shown to be involved in the process of apoptosis, vascular smooth muscle cell differentiation, angiogenesis, and regeneration of cardiomyocytes [17]. [score:1]
b miR-133 level in exosome isolated from MSC culture supernatant. [score:1]
Previous studies reported an inconsistent modulatory effect of miR-133 on cell proliferation and differentiation through different signaling pathways [32, 33]. [score:1]
miR-133-MSCs effectively preserve cardiac function in a rat MI mo del. [score:1]
Histological assessment of heart slices revealed that cell apoptosis and inflammatory cell infiltration were ameliorated in miR-133-MSC -treated hearts (Fig.   5a). [score:1]
d Snail 1 3′UTR contains predicted miR-133 binding sites, which are conserved among species. [score:1]
CON control, NC negative control In order to determine whether miR-133 affected MSCs, we transfected MSCs with miR-133 agomir/antagomir. [score:1]
Thus, miR-133 secreted from MSCs might influence the biological functions of other cells. [score:1]
These data indicated that, in addition to promoting MSC survival, the improvement of cardiac function in the infarcted heart could be also mediated by miR-133 secreted from miR-133-MSCs. [score:1]
Fig. 3Construction of miR-133 lentivirus. [score:1]
Elevation of miR-133 reduced hypoxia -induced, oxidative stress -induced, and endoplasmic reticulum stress -induced cardiac apoptosis in vitro [19– 21]. [score:1]
Briefly, MSCs in 96-well plates were transfected with miR-133 agomir/antagomir and cultured for 6, 12, 24, and 48 h. The culture supernatants were then changed to fresh medium with 10% CCK-8 (Dojindo Laboratories, Japan). [score:1]
a Scatter diagram of apoptosis in MSCs transfected with miR-133 agomir, antagomir, or their corresponding negative control (NC). [score:1]
We assessed the in-vivo therapeutic effects of miR-133-MSCs on a rat MI mo del. [score:1]
MSCs (3 × 10 [5] cells) were seeded onto the 12 wells of a 12-well plate, incubated overnight, and then transfected with miR-133a agomir, miR-133a antagomir, or negative control using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions as described previously [3]. [score:1]
Thus, we chose 24-h treatment to further study the influence of miR-133 on hypoxia -induced MSC apoptosis. [score:1]
c Morphology of MSCs transfected with miR-133 lentivirus (upper panel, bright field; lower panel, fluorescence field). [score:1]
Our study aim was to evaluate the therapeutic efficacy and mechanisms of miR-133 -overexpressing mesenchymal stem cells (MSCs) on acute myocardial infarction. [score:1]
On the contrary, miR-133a antagomir significantly facilitated hypoxia -induced MSC apoptosis (Fig.   2a, b). [score:1]
By the method of hypoxia, a wi dely used in-vitro mo del to mimic the ischemic myocardium microenvironment, we first revealed that miR-133 agomir could significantly reduce hypoxia -induced MSC apoptosis at both early (14.89% versus 25.14% in miR-133 agomir NC) and late (2.54% versus 6.15% in miR-133 agomir NC) stages. [score:1]
CFSE carboxyfluorescein diacetate succinimide ester, CON control, NS not significant, PARP poly ADP-ribose polymerase, PI propidium iodide However, no obvious change in cell-cycle distribution (Fig.   2d), cell viability (Fig.   2f and 1: Figure S1B), and cell proliferation (Fig.   2g and 1: Figure S1c) was detected in MSCs transfected with control miRNA, miR-133 agomir, or miR-133 antagomir. [score:1]
miR-133 Mesenchymal stem cells Myocardial infarction Myocardial infarction (MI), arising from myocardial ischemia, is the leading cause of morbidity and mortality in the world [1]. [score:1]
The improved cardiac function in the miR-133-MSC group was partially caused by increased survival of transplanted MSCs, as indicated by CM-Dil staining. [score:1]
miR-133 enhanced survival of MSCs under hypoxic conditions. [score:1]
These data confirmed that MSCs were successfully isolated and modulated with miR-133 agomir/antagomir. [score:1]
miR-133-MSCs obviously improved cardiac function in a rat mo del of myocardial infarction. [score:1]
MSCs were transfected with miR-133 agomir, miR-133 antagomir, or negative control, and subsequently cultured in DMEM/F12 with exosome-free FBS. [score:1]
miR-133-MSCs effectively reduce inflammation and fibrosis in the MI mo del. [score:1]
Thus, miR-133 secreted by miR-133-MSCs may enhance the function of the infarcted heart through reducing inflammation and fibrosis. [score:1]
Forty-eight hours later, the isolated cardiomyocytes were cocultured with MSCs transfected with miR-133 agomir/miR-133 antagomir or negative control at a 10:1 ratio. [score:1]
CON control, NC negative control In order to determine whether miR-133 affected MSCs, we transfected MSCs with miR-133 agomir/antagomir. [score:1]
In this study, we found miR-133 had little influence on proliferation of MSCs. [score:1]
Our study demonstrated that both early and late apoptosis were obviously decreased in MSCs transfected with miR-133a agomir. [score:1]
CFSE carboxyfluorescein diacetate succinimide ester, CON control, NS not significant, PARP poly ADP-ribose polymerase, PI propidium iodide However, no obvious change in cell-cycle distribution (Fig.   2d), cell viability (Fig.   2f and 1: Figure S1B), and cell proliferation (Fig.   2g and 1: Figure S1c) was detected in MSCs transfected with control miRNA, miR-133 agomir, or miR-133 antagomir. [score:1]
Consistently, miR-133 antagomir accelerated cell apoptosis of MSCs under hypoxic conditions. [score:1]
The vector pCDH-CMV-MCS-EF1-copGFP was used as a backbone plasmid to reconstruct lentiviral vector containing miR-133a. [score:1]
1:Is Figure S1 showing influence of miR-133 on apoptosis, viability, and proliferation at different times on MSCs. [score:1]
MSCs at passage 5 were placed in a 12-well plate at a confluence of 80% and then transfected with miR-133 agomir/antagomir or negative controls. [score:1]
Fragments of rat pre-miR-133 (281 bp) were amplified by PCR from rat genomic DNA (Fig.   3a). [score:1]
The vector and pre-miR-133a fragments amplified from rat genomic DNA were digested with XbaI and EcoRI (NEB, USA) and ligated with T4 ligase (TAKARA). [score:1]
a Electrophoretogram of pre-miR-133 fragments. [score:1]
For lentiviral production, HEK293NT cells were cotransfected with control vector or lentiviral plasmid carrying pre-miR-133 fragments, along with lentiviral packaging mix. [score:1]
MSC infection with miR-133a lentivirus. [score:1]
b Fluorescence image of GFP [+] 293NT infected with lentivirus carrying pre-miR-133. [score:1]
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[+] score: 196
Other miRNAs from this paper: rno-mir-133b, rno-mir-133c
Our results showed that APN reversed miR-133a expression level downregulated by Ang II in vivo and in vitro. [score:6]
APN upregulated miR-133a levels through inhibiting ERK1/2 phosphorylation. [score:6]
APN upregulated miR-133a levels by inhibiting ERK1/2 phosphorylation. [score:6]
In addition, mir-133a also decreased significantly while using the AMPK inhibitor compound c or lentiviral AMPK shRNA alone, suggesting an important effect of AMPK pathway on miR-133a expression. [score:5]
Although several studies have demonstrated that APN inhibits cardiac hypertrophy[15, 19– 22], whether APN has an effect on miR-133a expression is unknown. [score:5]
According to TargetScan prediction results, there are 400–500 putative mRNA targets for miR-133a. [score:5]
The miR-133a expression level was normalized to U6 expression following the ΔΔCT method. [score:5]
The disease -associated profiles of miR-133a expression could be generated in response to hypertrophic stimuli elicited by variations in the activity of intracellular signaling pathways. [score:5]
In our study, APN inhibited the increased CTGF expression induced by Ang II, which may be one reason for the modulation of miR-133a and the protection role of APN. [score:5]
However, transgenic expression of miR-133a inhibited myocardial fibrosis and improved diastolic function without affecting the extent of hypertrophy in pressure-overloaded adult hearts [51]. [score:5]
According to TargetScan prediction results, there are hundreds of mRNAs targeted by miR-133a. [score:5]
To further confirm the effect of AMPK on miR-133a expression, a lentiviral vector expressing AMPK short hairpin RNA (shRNA) was constructed and infected into NRVMs. [score:5]
In Esther E. Creemers’s study, the 3’-UTR of CTGF was proved to be a direct target of miR-133a[10]. [score:4]
In summary, this study shows for the first time that APN reverses miR-133a level which is downregulated by Ang II through AMPK activation, reduced ERK1/2 phosphorylation in cardiomyocytes, revealing a previously undemonstrated and important link between APN and miR-133a. [score:4]
Here, we show for the first time that APN could attenuate the downregulation of miR-133a induced by Ang II through AMPK activation, reduced ERK1/2 phosphorylation, revealing a previously undemonstrated and important link between APN and miR-133a. [score:4]
Ang II downregulate miR-133a level in a dose and time- dependent manner. [score:4]
Thus, we next detected whether APN prevented the downregulation of miR-133a through the ERK1/2 pathway. [score:4]
Furthermore, miR-133 expression was also negatively regulated by the ERK1/2 signaling pathway. [score:4]
CTGF is a direct target of miR-133a[10]. [score:4]
CTGF was shown to be a direct target of miR-133a in the previous study[10]. [score:4]
In their study, downregulation of ERK1/2 phosphorylation by miR-133 was detected. [score:4]
In the present study, we show that APN reversed the downregulation of miR-133a stimulated by Ang II through the AMPK and ERK1/2 pathway in NRVMs. [score:4]
These results indicated that APN reversed the miR-133a downregulation induced by Ang II by ameliorating ERK1/2 phosphorylation. [score:4]
When pretreating NRVMs with the ERK1/2 inhibitor PD98059 (30 μM) for 1 hour before stimulation with Ang II, we observed that miR-133a expression increased significantly compared with the Ang II treatment group (Fig 5B). [score:4]
In addition, by using the ERK1/2 inhibitor PD98059 alone could also elevate the miR-133a level, suggesting that ERK1/2 may involve in the regulation of miR-133a in heart. [score:4]
APN reversed miR-133a downregulation by Ang II. [score:4]
However, whether miR-133a upregulation by APN occurred through the AMPK pathway was not known. [score:4]
APN upregulated miR-133a through AMPK pathway in the Ang II mediated hypertrophic responses. [score:4]
Our results show that APN upregulates miR-133a through AMPK activation. [score:4]
In previous studies, miR-133a was found to be specifically expressed in cardiac and skeletal muscle and proved to play a key role in skeletal and cardiac muscle development and function. [score:4]
APN attenuated cardiac hypertrophy in vitro and reversed miR-133a downregulation by Ang II in vivo and in vitro. [score:4]
The positive effect of APN on AMPK phosphorylation and miR-133a, and inhibitory effect on ERK phosphorylation was dramatically attenuated in NRVMs transfected with lentiviral AdipoR1 shRNA (Fig 6B–6D). [score:3]
However, whether APN modulates miR-133a expression is unknown. [score:3]
To determine which receptor was responsible for the effect of APN on miR-133a in Ang II induced cardiac hypertrophy, we firstly detected AdipoR1 and AdipoR2 mRNA expression in NRVMs stimulated with Ang II. [score:3]
MiR-133a is downregulated in cardiac hypertrophic responses. [score:3]
Here, we hypothesized that APN may affect miR-133a expression in Ang II induced cardiac hypertrophy. [score:3]
The results demonstrated that as an activator of AMPK, APN increased miR-133a level which was suppressed by Ang II. [score:3]
To determine the effect of Ang II on miR-133a expression, NRVMs were stimulated with 50, 100, 200, 500 nM Ang II for 24 h, or with 100 nM Ang II for 3, 6, 12, 24, 48 h. The results showed that miR-133a was repressed significantly in a dose and time -dependent manner in NRVMs stimulated Ang II (S3 File). [score:3]
The AMPK inhibitor compound c (20 μM) weakened the effects of APN, and 30 μM compound c canceled the effect of APN on miR-133a. [score:3]
NRVMs transduced with lentiviral AMPK shRNA canceled the effect of APN on miR-133a, indicating that APN may regulate miR-133a through the AMPK pathway (Fig 4). [score:2]
However, whether ERK1/2 involved in APN mediated regulation of miR-133a in cardiac hypertrophy is unknown. [score:2]
AMPK activation and reduced ERK1/2 phosphorylation were responsible for APN positive regulation on miR-133a. [score:2]
According to the previous studies, a few factors have been identified involved in the regulation of miR-133a, such as serum response factor (SRF)[45], MEF2 [46] and IP3[42]. [score:2]
In S-H Zhao’s study, a new feedback loop between miR-133 and the ERK1/2 signaling pathway involving an exquisite mechanism for regulating myogenesis was revealed in C2C12 (Mouse myoblast cell line) cells [6]. [score:2]
To further test whether AMPK activation was responsible for miR-133a regulation by APN, we determined the miR-133a level in NRVMs following the treatments indicated in Fig 4B. [score:2]
Knockdown of miR-133a was sufficient to induce cardiac hypertrophy[8]. [score:2]
These results indicated AMPK was an important mediator in the regulation of miR-133a. [score:2]
Thus, a network of genes can be subject to coordinated and simultaneous regulation by miR-133a. [score:2]
In the human heart, miR-133a is the most abundant miRNA and is involved in the regulation of cardiac hypertrophy and failure [5]. [score:2]
These data may provide new evidence for the regulation of miR-133a. [score:2]
However, whether AMPK is involved in the regulation of miR-133a is unknown. [score:2]
These results provide new evidence for the mechanism underlying cardiac hypertrophy and may provide important insight into regulatory networks of miR-133a, revealing a previously undemonstrated and important link between APN and miR-133a. [score:2]
Recombinant rat APN pretreatment (5 μg/ml) markedly attenuated the miR-133a reduction caused by Ang II (100 nM) stimulation for 24h (Fig 3E). [score:1]
The miR-133a and U6 expressions were evaluated by real-time PCR using the ABI PRISM 7900 Sequence Detection System. [score:1]
APN reversed the miR-133a reduction in the Ang II mediated hypertrophic response via the AMPK pathway. [score:1]
According to these results, we speculate that APN may also affect other miR-133a target proteins in the heart, which need further investigation. [score:1]
We next sought to examine whether the positive effect of APN on miR-133a was mediated by AMPK. [score:1]
Thus, we speculate that APN plays a protective role in myocardial partly through its positive effect on miR-133a. [score:1]
S3 FileqRT-PCR was performed to detect miR-133a level under different treatment (**, p < 0.01 vs control). [score:1]
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In addition, we observed an increased expression of Nix in the soleus of rats exposed to the HFS diet or gestational diabetes (Figure 7f), concurrent with increased expression of the catalytic fragment of PKC δ. These findings suggest that developmental programming of diacylglycerol metabolism and miR-133a expression influences mitochondrial markers, and Nix expression, in the offspring. [score:10]
In addition, when miR-133a was expressed in myoblasts, we did not detect a change in Nix mRNA, suggesting that miR-133a inhibits Nix expression by translational block rather than mRNA degradation. [score:9]
Palmitate -induced mitochondrial depolarization involves PKC δ and inhibition of miR-133a expressionGiven the recently described role of miR-133a in regulating muscle mitochondrial respiration, [19] we hypothesized that palmitate -induced mitochondrial dysfunction involves PKC δ -dependent miR-133a inhibition. [score:8]
Thus, we expressed miR-133a in cultured myoblasts, and observed reduced protein expression of Nix, where a shRNA targeting Nix (shNix) was used as a positive control (Figure 5b). [score:7]
Next, we evaluated whether the endogenous expression of miR-133a by MEF2C and SRF was regulated by PKC δ. When the catalytic fragment of PKC δ was co-expressed with MEF2C and SRF, the induction of miR-133a was inhibited in differentiating C2C12s (Figure 3b). [score:6]
These findings suggest a degree of functional dependency between MEF2C and SRF in the regulation of miR-133a expression that is consistent with our promoter analysis in Supplementary Figure 1. Previously, it was demonstrated that PKC δ phosphorylates SRF at threonine-160 to inhibit DNA binding. [score:6]
These findings suggest a degree of functional dependency between MEF2C and SRF in the regulation of miR-133a expression that is consistent with our promoter analysis in Supplementary Figure 1. Peptide mapping of PKC δ phosphorylation of MEF2 and SRF by mass spectrometryPreviously, it was demonstrated that PKC δ phosphorylates SRF at threonine-160 to inhibit DNA binding. [score:6]
Repression of miR-133a expression ultimately regulates mitochondrial function, through the Bcl-2 family member Nix, which may have implications to pathological states such as insulin resistance and cardiovascular disease. [score:6]
To perform the reciprocal experimentation, we utilized a miR-133a inhibiting oligonucleotide, and observed increased expression of Nix protein (Figure 5c). [score:5]
This screen identified a conserved miR-133a target sequence in the 3'-untranslated region of the human and rodent Nix mRNA (Figure 5a). [score:5]
Correspondingly, palmitate treatment reduced miR-133a expression, which was reversed by PKC δ inhibition by rottlerin (Figure 4d). [score:5]
To assess the role of miR-133a in palmitate -induced mitochondrial depolarization mechanistically, we transfected C2C12 myoblasts with an inhibitory oligonucleotide targeting miR-133a. [score:5]
Furthermore, when C2C12 cells were transfected with T20A-VP16, palmitate treatment was unable to inhibit miR-133a expression (Figure 3e). [score:5]
The combination of MEF2C and SRF induced endogenous miR-133a expression in differentiating C2C12 myotubes (Figure 1a), and we confirmed that ectopic expression of MEF2C and SRF was maintained at this timepoint (Supplementary Figure 2). [score:5]
Palmitate -induced mitochondrial depolarization involves PKC δ and inhibition of miR-133a expression. [score:5]
In summary, these studies document a novel signaling cascade triggered by lipotoxicity, and converging on MEF2 and SRF transcription factors to regulate the expression of miR-133a during muscle development and post-natal remo deling. [score:5]
Interestingly, miR-133a has been shown to target both SRF and MEF2C, which suggests an element of feedback controlling the expression of this microRNA. [score:5]
Given the recently described role of miR-133a in regulating muscle mitochondrial respiration, [19] we hypothesized that palmitate -induced mitochondrial dysfunction involves PKC δ -dependent miR-133a inhibition. [score:4]
Downstream, collaborative regulation of miR-133a expression by MEF2C and SRF is attenuated by PKC δ phosphorylation of these transcription factors. [score:4]
Knockdown of MEF2C or SRF individually reduced the endogenous expression of miR-133a in differentiating myotubes (Figure 1b). [score:4]
Interestingly, simultaneous knockdown of both MEF2C and SRF did not additively reduce miR-133a expression (Figure 1b). [score:4]
MEF2C and SRF regulate the endogenous expression of miR-133a. [score:4]
To identify a mechanism by which miR-133a regulates mitochondrial function, we performed an in silico screen in an attempt to identify novel mRNA targets of miR-133a. [score:4]
As shown in Figure 4i, cells expressing miR-133a were resistant to palmitate -induced disruption of mitochondrial membrane potential. [score:3]
Importantly, expression of either miR-133a or an active MEF2 fusion protein, which cannot be phosphorylated by PKC δ, reverses palmitate -induced mitochondrial dysfunction. [score:3]
Thus, we hypothesized that the accumulation of diacylglycerol species would provide an activating stimulus for PKC δ. In support of this, we observed that miR-133a expression was reduced by 40% in the soleus and heart of animals exposed to both gestational diabetes and a HFS diet (Figures 7b and c). [score:3]
One of the most intriguing findings of the present study is the identification of Nix as a miR-133a target. [score:3]
To determine the effect of an endogenous activator of PKC δ on miR-133a expression, we exposed cells to the saturated fatty acid palmitate. [score:3]
Concurrently, we observed reduced expression of miR-133a (Figure 3d). [score:3]
Previous studies have implicated both Nix and miR-133a in the regulation of mitochondrial function and programmed cell death in multiple cell types, 19, 35, 36, 37 and our data strongly suggest that miR-133a is dependent on Nix for mitochondrial membrane potential regulation in muscle tissues. [score:3]
Importantly, either factor alone had no effect, and MEF2A did not activate miR-133a expression. [score:3]
As shown in Figure 4e, myotubes transfected with the miR-133a inhibitor displayed a reduced TMRM fluorescence, but an equivocal MitoTracker fluorescence, compared with control myotubes (Figures 4g and h). [score:2]
For this we chose miR-133a, given that it has been recently identified as a regulator of muscle growth and metabolic function. [score:2]
However, regulation of MEF2 and SRF by phosphorylation at the conserved MADS-box motif, and its downstream effects on miR-133a and Nix, may have evolved to limit mitochondrial metabolism and divert nutrients to anabolic storage or cell growth during differentiation. [score:2]
miR-133a regulates mitochondrial function through the mitophagy and death gene Nix. [score:2]
Evaluation of miR-133a and Nix expression in vivoTo determine the in vivo relevance of this genetic pathway in muscle tissues, we utilized a rodent mo del of gestational diabetes, as fetal exposure to diabetes during pregnancy increases the risk for early-onset insulin resistance in the offspring and may program metabolism. [score:1]
Evaluation of miR-133a and Nix expression in vivo. [score:1]
Furthermore, both Nix and miR-133a are involved in pathological cardiac remo deling. [score:1]
Next, we transfected myoblasts with a plasmid encoding miR-133a in order to reconstitute this microRNA's function in palmitate -treated cells. [score:1]
[32] However, when cells were transfected with a miR-133a mimicking oligonucleotide, the palmitate -induced drop in oxygen consumption was prevented (Figure 6b), where control cells were transfected with a scrambled oligonucleotide. [score:1]
The miR-133a expression plasmid was purchased from Addgene (Principal Investigator David Bartel, plasmid 26326). [score:1]
As shown in Figures 6e and f, overnight exposure to palmitate prevented insulin-stimulated glucose uptake in differentiated H9c2 cells, determined by the fluorescence glucose analog 2NBDG, which was restored when cells were treated with a miR-133a mimic. [score:1]
Interestingly, basal glucose uptake was also increased in cells treated with the miR-133a mimic and exposed to palmitate. [score:1]
[1 to 20 of 43 sentences]
4
[+] score: 159
It was found that IPost enhanced the expression of miR-133a during IR, and that CASP9 protein was up-regulated by IR and down-regulated by IPost. [score:9]
We also found that miR-133a was down-regulated by IR and up-regulated by IPost, which is consistent with other reports [14, 15, 28, 31]. [score:7]
It was found that the expression of CASP9 protein was uperegulated by AMO-133a and down-regulated by miR-133a mimic (P < 0.05, Figure 8). [score:7]
For example, miR-208 was up-regulated, while miR-1 and miR-133a were down-regulated in MI [14]. [score:7]
In addition, CASP9 protein was down-regulated by miR-133a mimic and up-regulated by AMO-133a. [score:7]
MiRNA-microarray and RT-PCR showed that myocardial-specific miR-1 and miR-133a were down-regulated by IR, and up-regulated by IPost compared with IR. [score:6]
IPost down-regulated CASP9 compared with IR, while miR-133a mimic down-regulated CASP9 protein and attenuated cardiomyocyte apoptosis induced by IR. [score:6]
AMO-133a up-regulated CASP9 protein, and miR-133a mimic down-regulated it(n = 10, *P < 0.05, compared with IR group). [score:6]
MiR-133a was down-regulated by AMO-133a, and up-regulated by miR-133a mimic (n = 10, *P < 0.05, compared with IR group; [▲]P < 0.05, compared with AMO-133+IR group); (B) The relative quantity of CASP9 protein in different groups. [score:5]
We therefore speculate that miR-133a has a protective effect against IR, and can attenuate myocardiocyte apoptosis by targeting CASP9, and that IPost can enhance miR-133a expression to reduce cardiomyocyte apoptosis. [score:5]
MiR-133a mimic down-regulated CASP9 protein expression and attenuated IR -induced apoptosis. [score:5]
According to the bioinformatics of Targetscan, CASP9 was a potential target of miR-133a. [score:5]
MiR-1 and miR-133a were down-regulated in IR group, while IPost up-regulated them as compared with IR group (n = 10, *P < 0.05, compared with Con group; [▲]P < 0.05, compared wit IR group). [score:4]
And up-regulation of miR-1 and miR-133a can decrease cardiomyocyte apoptosis. [score:4]
It was found that myocardial-specific miR-1 and miR-133a were down-regulated after IR. [score:4]
It was reported that miR-133 exhibited an anti-apoptotic effect in IR by regulating the expression of CASP9 [15]. [score:4]
IPost can up-regulate miR-1 and miR-133a, and decrease apoptosis of cardiomyocyte. [score:4]
The most significant findings are up-regulation of miR-1 and miR-133a in IPost compared with IR hearts. [score:3]
IPost up-regulated miR-1 and miR-133a compared with IR (P < 0.05, Figure 5). [score:3]
The results of flow cytometry and TUNEL assay showed that up-regulation of miR-1 and miR-133a decreased apoptosis of cardiomyocytes. [score:3]
So we selected CASP9 as the potential target protein of miR-133a to see whether miRNA was involved in the anti-apoptotic effect of IPost against IR injury. [score:3]
Figure 8 The expression of miR-133a and CASP9 protein after transferring the mimic or AMO. [score:3]
We found that CASP9 was a potential target of miR-133a. [score:3]
Among the miRNAs, miR-1 and miR-133 are specifically expressed in cardiac and skeletal muscles [14, 15]. [score:3]
MiR-133a can also regulate cardiac rhythms by targeting HCN2 and HCN4 [34]. [score:3]
CASP9 was not only the potential target protein of miR-133a but the important pro-apoptotic factor during IR [35]. [score:3]
MiR-133a regulates the protein expression of CASP9. [score:3]
MiR-1 promoted cell aopoptosis during IR, but miR-133a inhibited cell apoptosis during IR. [score:3]
MiRNA-1 and miRNA-133a regulate apoptosis of cardiomyocytes. [score:2]
MiR-133a may attenuate apoptosis of myocardiocytes by targeting CASP9. [score:2]
CASP9, as one of the candidate target of miR-133a, was compared during IR after the miR-133a mimic or AMO-133a was transferred into the myocardium. [score:2]
Myocardial-specific miR-1 and miR-133a may play an important role in IPost protection by regulating apoptosis-related genes. [score:2]
Figure 5 Regulation of miR-1 and miR-133a by IPost. [score:2]
In summary, our results confirm that myocardial-specific miR-1 and miR-133a play an important role in IPost protection against myocardial IR injury by regulating apoptosis-related genes. [score:2]
Dysregulated miR-1 and miR-133a were validated by quantitative real-time RT-PCR in duplicates using Rotor Gene 3000 (Corbett Research, Sydney, Australia). [score:2]
To see whether miR-133a regulated cell apoposis induced by IR in vivo, miR-133a mimic or AMO-133a was transferred into the myocardium before IR. [score:2]
The present study was undertaken to see whether miRNAs, especially myocardial-specific miR-1 and miR-133a, were involved in the protective effect of myocardial IPost by regulating apoptosis-related genes. [score:2]
MiR-133a is essential in orchestrating cardiac development [33]. [score:1]
MiR-1 and miR-133 produced opposing effects on apoptosis induced by H [2]O [2 ][15]. [score:1]
: rno-miR-1, NR 032116.1; rno-mir-133a, NR 031879.1) and AMOs (AMO-1 and AMO-133a) were synthesized by Jima Inc (Shanghai, China). [score:1]
After transferring miR-133a mimic and AMO-133a into the cultured neonatal cardiomyocytes and myocardium, we found that miR-133a mimic attenuated apoptosis, and AMO-133a promoted apoptosis, as shown by flow cytometry and TUNEL. [score:1]
Treatment with miR-1 or miR-133a mimic significantly decreased AP of cardiomyocytes induced by IR, while IR -induced apoptosis was increased by AMO-1 or AMO-133a pretreatment. [score:1]
The annealing temperature of miRNA-1 and miRNA-133a was set at 60°C, and that of Bcl-2 and Bax was set at 58°C. [score:1]
The sequences of miRNA mimics and AMOs are showed in Table 2. Table 2 The sequences of miRNA mimics and AMOs miR-1 mimic 5'-UGGAAUGUAAAGAAGUGUUAUACACACUUCUUUACAUUCCAUU-3' AMO-1 5'-AUACACACUUCUUUACAUUCCA-3' miR-133a mimic 5'-UUUGGUCCCCUUCAACCAGCUGGCUGGUUGAAGGGGACCAAAUU-3' AMO-133a 5'-CAGCUGGUUGAAGGGGACCAAA-3' were performed as previously described [22]. [score:1]
MiR-133a and miR-1 are clustered on the same chromosome loci and transcribed together in a tissue-specific manner [32]. [score:1]
The sequences of miRNA mimics and AMOs are showed in Table 2. Table 2 The sequences of miRNA mimics and AMOs miR-1 mimic 5'-UGGAAUGUAAAGAAGUGUUAUACACACUUCUUUACAUUCCAUU-3' AMO-1 5'-AUACACACUUCUUUACAUUCCA-3' miR-133a mimic 5'-UUUGGUCCCCUUCAACCAGCUGGCUGGUUGAAGGGGACCAAAUU-3' AMO-133a 5'-CAGCUGGUUGAAGGGGACCAAA-3' Mimic and AMO of miRNA pretreatment in vivo were performed as previously described [22]. [score:1]
These results indicated that miR-1 and miR-133a had a cytoprotective effect against IR -induced apoptosis (P < 0.05, Figure 10). [score:1]
To demonstrate the effect of miR-1 and miR-133a on IR -induced apoptosis of cardiomyocytes, miRNA's mimics and AMOs (50 nM) were transferred into the cardiomyocytes with lipofectamine 2000 (Invitrogen) 48 h before IR. [score:1]
With the chest open as described above, 100 ul synthesized miR-133a mimic or AMO-133a (50 mg/Kg), pretreated with lipofectamine 2000 (Invitrogen), was injected into the myocardium. [score:1]
It was found that miR-133a mimic decreased the apoptosis ratio induced by IR, while AMO-133a increased the apoptosis ratio (P < 0.05, Figure 9). [score:1]
[1 to 20 of 50 sentences]
5
[+] score: 136
Other miRNAs from this paper: rno-mir-1, rno-mir-133b, rno-mir-133c
Indeed, we demonstrated that SIRT1 was a direct target of miR-133a that downregulated SIRT1 expression. [score:9]
We further demonstrated that hypoxia stimulated miR-133a promoter activity and upregulated miR-133a expression in the heart, which in turn suppressed SIRT1 by binding to its transcript 3′UTR. [score:8]
As shown in Figure 9C, although the negative control had no effect on hypoxia -induced downregulation of SIRT1 protein abundance, the effect of hypoxia was blocked by the inhibition of miR-133a with the inhibitor miR-133a-LNA. [score:8]
We identified that microRNA-133a (miR-133a), a miR specifically expressed in cardiac muscle [26, 27] and involved in cardiomyocyte proliferation [28, 29], was upregulated by hypoxia due to a classical hypoxia response element (HRE) present in the promoter of miR-133a. [score:6]
The present study suggests a new mechanism by which miR-133a regulates cardiomyocyte terminal differentiation via suppressing SIRT1 expression. [score:6]
Hypoxia upregulated miR-133a expression. [score:6]
In contrast, the expression of miR-133a, a heart specific miRNA, was high in fetal hearts but significantly decreased in P7 hearts (Figure 4C), suggesting a possible role of miR-133a in the regulation of SIRT1 expression in the developing heart. [score:6]
Given that fetal development takes place in a hypoxic environment and miR-133a expression is high in the fetal heart, we sought to examine whether miR-133a was regulated by hypoxia. [score:5]
The finding of an inverse relationship between SIRT1 and miR-133a expression patterns in the developing heart is of interest and suggests a regulation of SIRT1 by miR-133a during the heart development. [score:5]
Similarly, it was reported that miR-133 targeted SIRT1 in glioma cells, leading to inhibition of cell proliferation [50]. [score:5]
In addition, a previous study showed that miR-133a regulated cardiac cell proliferation via inhibiting cyclin D2 [51], which may also play a role in cardiomyocyte differentiation. [score:4]
We then determined whether this hypoxia -induced downregulation of SIRT1 was mediated by miR-133a. [score:4]
MiR133a binds to SIRT1 mRNA 3′UTR and inhibits SIRT1 protein expression. [score:4]
In the present study, we found that miR-133a was significantly upregulated in both fetal hearts and cardiomyocytes exposed to hypoxia, which coincides with the fact that the in utero environment is naturally hypoxic. [score:4]
MiR-133a directly targeted SIRT1 3′UTR. [score:3]
Effect of hypoxia on miR-133a expression in fetal hearts and cardiomyocytes. [score:3]
At the same time, we showed that mature miR-133a expression was high in fetal hearts, but significantly reduced in the hearts of day 7 pups. [score:3]
Hearts were isolated from near-term (E21) fetuses and P7 pups and SIRT1 expression and miR133a abundance were determined. [score:3]
Thus, the present study reveals a novel role of SIRT1, and its regulation by miR-133a, in cardiomyocyte terminal differentiation in the heart development. [score:3]
Figure 4Hearts were isolated from near-term (E21) fetuses and P7 pups and SIRT1 expression and miR133a abundance were determined. [score:3]
Overall, the present study demonstrates for the first time an axis of hypoxia-miR-133a-SIRT1 in the regulation of cardiomyocyte terminal differentiation during the heart development. [score:3]
Of importance, the present study revealed that SIRT1 was a downstream target of miR-133a and the 3′UTR of SIRT1 transcript harbored a miR-133a recognition sequence. [score:3]
As shown in Figure 5A, the miR-133a-3p mimic produced a dose -dependent inhibition of reporter activity of the pmiRGLO-SIRT1 reporter construct, whereas the negative control had no effect. [score:3]
Expression of SIRT1 and miR133a in the developing heart. [score:3]
Thus, these findings implicate miR-133a/SIRT1 as key regulators in cardiomyocyte terminal differentiation and maturation during the heart development. [score:3]
Expression of SIRT1 and miR-133a in fetal and neonatal hearts. [score:3]
To determine if the interaction between miR-133a-3p mimic and SIRT1 mRNA is direct, we created a pmiRGLO-SIRT1 reporter construct and transfected H9c2 cells with the reporter construct. [score:2]
Figure 5(A) SIRT1 mRNA 3′UTR shows complementary binding sequences to the seed sequences of rat miR133a. [score:1]
To determine whether hypoxia indeed increased miR-133a in the heart in vivo, pregnant rats were treated with hypoxia (10.5% O [2]) from days 15 to 21 of gestation. [score:1]
MiR133a expression was measured by miScript miR real-time RT-qPCR. [score:1]
MiRNA-133a has been shown to play an important role in cardiac development [29]. [score:1]
MiR-1 and miR-133a are coded by a bicistronic promoter [29]. [score:1]
The oligonucleotide probes containing HBS (sense: 5′-ctgggaaatgtgagtggaaacatgag; anti-sense: 5′-ctcatgtttccactcacatttcccag) and HAS (sense: 5′-gaaacatgagacacgtctttatttggca; anti-sense: 5′-tgccaaataaagacgtgtctcatgtttc) motifs in the miR-133a promoter were biotin-labeled and then subjected to EMSA using LightShift Chemiluminescent EMSA Kit (Pierce Biotechnology). [score:1]
MiR-133a promoter was regulated by hypoxia response element (HRE). [score:1]
A 412-bp segment of 3′UTR of rat SIRT1 mRNA containing the miR-133a binding sequence was PCR amplified as previously described [61]. [score:1]
H9c2 cells were transfected with pmiRGLO vector containing putative miR133a binding sites within the SIRT1 3′UTR (pmiRGLO-SIRT1) and co -transfected with miR133a mimic or negative control scramble for 48 hours. [score:1]
n = 6 [*] P < 0.05, miR133a mimic versus pmiRGLO-SIRT1 alone. [score:1]
n = 4 [*] P < 0.05, miR133a mimic versus negative control. [score:1]
We identified a rat miR-133a recognition motif in the rat sirtuin 1 (SIRT1) transcript 3′UTR. [score:1]
This was further demonstrated by the results showing that the miR-133a-3p mimic treatment significantly decreased SIRT1 protein abundance in H9c2 cells (Figure 5B). [score:1]
This bicistronic promoter drives the transcription of two heart specific microRNAs, namely miR-1 and miR-133a. [score:1]
As shown in Figure 8B, hypoxia significantly increased miR-133a in primary cardiomyocytes. [score:1]
The present study provides evidence of a novel mechanism of miR-133a/SIRT1 through which changing oxygen levels affect the timing of cell-cycle withdrawal in the developing heart. [score:1]
Figure 8(A) Hearts were isolated from E21 fetuses from pregnant rats treated with normoxia or hypoxia (10.5% O [2]) from day 15 to day 21 of gestation, and miR133a expression was measured by miScript miR real-time RT-qPCR. [score:1]
We identified a miR-133a-3p recognition motif in the rat SIRT1 transcript 3′UTR (Figure 5A). [score:1]
[1 to 20 of 45 sentences]
6
[+] score: 114
In the present study, we found that the expression of microRNA-133a was down-regulated both in Dahl SS rats and in SD rats, so we speculate that high-salt was likely to down-regulated microRNA expression via its effect on RAAS system in heart tissue. [score:11]
Castold [13] showed that microRNA-133a could inhibit collagen I expression at the translation level by targeting three untranslated binding sites. [score:11]
Using a nicotine -induced atrial fibrosis mo del [11], another study has demonstrated that microRNA-133a directly suppresses TGF-β expression, and that TGF-β is a upstream regulator of CTGF. [score:7]
The findings of the present study suggest that up-regulation of microRNA-133a may suppress myocardial fibrosis in salt-sensitive hypertension. [score:6]
In the current study, we found that high-salt suppresses myocardial microRNA-133a expression and increases the level of CTGF and collagen I. More studies are needed to confirm the role of microRNA-133a in salt-sensitive hypertension, and to determine whether or not it directly acts on all the three factors. [score:6]
Myocardial down-regulation microRNA-133a may represent a regulatory mechanism that leads to myocardial fibrosis. [score:5]
2009.01.002 19167326 6. Liu N. Bezprozvannaya S. Williams A. H. Qi X. Richardson J. A. Bassel-Duby R. Olson E. N. MicroRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart Genes Dev. [score:5]
Another study confirmed that microRNA-133 directly regulates the expression of transforming growth factor β (TGF-β) [11], connective tissue growth factor (CTGF) [12] and collagen I [13] in different mo dels. [score:5]
After high-salt intervention, microRNA-133a in the SD rats was suppressed by nearly 50%, but the expression of cardiac CTGF and collagen I did not increase correspondingly. [score:5]
The expression of microRNA-133a is found to be negatively correlated with the expression of CTGF. [score:5]
This study demonstrates that high-salt intake could suppress the expression of myocardial microRNA-133a partly independent of its effect on blood pressure. [score:5]
Recently, Castold [13] showed that AngII could suppress microRNA-133a expression via AT1 receptor. [score:5]
However, very few reports have focused on whether high salt intake could regulate the expression of microRNA-133a and promote myocardial fibrosis. [score:4]
Duisters [12] observed the downregulation of microRNA-133a in a mouse mo del of transverse aortic constriction and in the pathological ventricular hypertrophy of human beings. [score:4]
For our analysis, compared with Dahl SS rats, SD rats were insensitive to high-salt intervention, a period of 4 weeks of high-salt intervention could suppress the expression of microRNA-133a, but it is not enough to cause an increase in myocardial collagen I in SD rats. [score:4]
Shan H. Zhang Y. Lu Y. Pan Z. Cai B. Wang N. Li X. Feng T. Hong Y. Yang B. Downregulation of miR-133 and miR-590 contributes to nicotine -induced atrial remo delling in canines Cardiovasc. [score:4]
Studies have shown that microRNA-133a is mainly expressed in cardiac and skeletal muscles. [score:3]
They identified three specific targets of microRNA-133a, namely, RhoA, Cdc42 and Nelf-A/WHSC2. [score:3]
High-salt intake decreased the expression of microRNA-133a in both strains (SS: 0.06 ± 0.01 vs. [score:3]
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of micrornas in myocardial matrix remo deling Circ. [score:2]
On the other hand, SBP of the SD rats was slightly elevated after high-salt intervention, so it indicated that high-salt intake could disturbed the expression of microRNA133a independently of its effect on blood pressure. [score:2]
Castoldi G. di Gioia C. R. T. Bombardi C. Catalucci D. Corradi B. Gualazzi M. G. Leopizzi M. Mancini M. Zerbini G. Condorelli G. mir-133a regulates collagen 1A1: Potential role of mir-133a in myocardial fibrosis in angiotensin II -dependent hypertension J. Cell. [score:2]
The myocardial tissue microRNA-133a, CTGF, and collagen I were detected through real-time PCR. [score:1]
Care et al. [10] demonstrated that microRNA-133a is involved in cardiac hypertrophy. [score:1]
The current study aims to observe the influence of high-salt intake on blood pressure, left ventricular weight, myocardial microRNA-133a and fibrosis levels by implementing high-salt diet intervention trial in Dahl salt-sensitive rats and SD rats. [score:1]
GAPDH was used as internal standard for CTGF and collagen I mRNA detection and U6 was used as internal standard for microRNA-133a detection. [score:1]
Figure 6Changes in mRNA for microRNA-133a in the four groups. [score:1]
Studies have shown that microRNAs are involved in many kinds of pathophysiologic process and both microRNA-133a and microRNA-1 are involved in cardiac hypertrophy and fibrosis [15]. [score:1]
The final objective is to discuss the role of microRNA-133a in salt-sensitive hypertensive cardiac fibrosis with high-salt intervention. [score:1]
[1 to 20 of 29 sentences]
7
[+] score: 107
We observed that approximately 1/10 of the recently identified 578 miRNAs are highly expressed in the mouse heart; SRF overexpression in the mouse heart resulted in altered expression of a number of miRNAs, including the down-regulation of mir-1 and mir-133a, and up-regulation of mir-21, which are usually dysregulated in cardiac hypertrophy and congestive heart failure [3, 13- 16]. [score:14]
In conclusion, our current study demonstrates that cardiac-specific overexpression of SRF leads to altered expression of cardiac miRNAs, especially the down-regulation of miR-1 and miR-133a, and up-regulation of miR-21, the dysregulation of which is known to contribute to cardiac hypertrophy. [score:12]
Real-time RT-PCR analysis revealed that mildly reduced SRF resulted in the down-regulation of miR-21 expression, but up-regulation of both miR-1 and miR-133a (Figure 5A). [score:9]
As shown in Figure 6, when pri-mir-1-1 and pri-mir-1-2 transcripts were down-regulated, so was miR-1 mature form; when pri-mir-133a1 and pri-mir-133a2 transcripts were down-regulated, the same was true for miR-133a mature form. [score:7]
Reducing cardiac SRF level using the antisense-SRF transgenic approach led to the expression of miR-1, miR-133a and miR-21 in the opposite direction to that of SRF overexpression. [score:6]
The up-regulation of miR-21, and the down-regulation of miR-1 and miR-133a were observed in SRF-Tg compared to wild-type (WT) mouse heart (P < 0.01**, n = 3). [score:6]
Our findings demonstrate for the first time that it is possible to regulate at the same time the expression of three miRNAs, miR-1, miR-133a and miR-21, through targeting the components of SRF -mediated signaling pathway. [score:6]
Interestingly, the down-regulation of miR-21, but up-regulation of miR-1 and mir-133a were observed in Anti-SRF-Tg compared to wild-type mouse heart (p < 0.01**, n = 3). [score:6]
When the mouse cardiac SRF level was reduced using the antisense-SRF transgenic approach, we observed an increase in expression of miR-1 and miR-133a miRNA, and a decrease in expression of miR-21. [score:5]
miR-1 ranks number 1 in expression, miR-133a ranks number 7 in expression. [score:5]
Our data revealed that the down-regulation of miR-1 correlates closely with that of miR-133a in the SRF-Tg at various time points from 7 days to 6 months of age (Figure 7B). [score:4]
Mir-1 and mir-133a are down-regulated in cardiac hypertrophy and cardiac failure, suggesting that they may play a role in the underlying pathogenesis [14, 43]. [score:4]
The down-regulation of miR-1 correlates closely with that of miR-133a in SRF-Tg at various time points from 7 days to 6 months of age (p < 0.05, n = 3 for all time points, except n = 6 for miR-21 at 6 months). [score:4]
The expression levels of miR-1, miR-133a and miR-21 were observed to be in the opposite direction with reduced cardiac SRF level in the Anti-SRF-Tg mouse. [score:4]
These findings suggest that SRF may regulate these two miRNAs at the level of polycistronic transcription, rather than at each individual miRNA (pri-mir-1 or pri-mir-133a) transcription, thereby keeping the expression of both miRNAs closely correlated. [score:4]
Another important miRNA, mir-133a, was ranked number seven in terms of level of expression. [score:3]
In addition, serum response factor (SRF), an important transcription factor, participates in the regulation of several cardiac enriched miRNAs, including mir-1 and mir-133a [4, 6]. [score:2]
Similarly, the mature miR-133a is derived from both mir-133a1 gene (on chromosome 18) and mir-133a2 gene (on chromosome 2). [score:1]
It is plausible that increasing mir-1 and mir-133a level at a specific time point may have potentially beneficial effects against the pathological conditions. [score:1]
Both miR-1 and miR-133a are produced from the same polycistronic transcripts, which are encoded by two separate genes in the mouse and the human genomes [42]. [score:1]
Both guide strand and passenger strand (*) of mir-133a are decreased in SRF-Tg vs. [score:1]
Matkovich et al reported that an increase of mir-133a level in the postnatal heart has beneficial effects against cardiac fibrosis after transverse aortic constriction [44]. [score:1]
Generally, the pri-miRNA transcript contains one miRNA (e. g pri-mir-21), but it can also contain more than one miRNAs (e. g. mir-1 and mir-133a). [score:1]
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8
[+] score: 85
If a substantial proportion of all miR-133a isomiRs expressed in normal myocardium is miR-133a(v) (as suggested by our data) then the downregulation of this variant could contribute to the upregulation of gelsolin in heart disease. [score:11]
Since miR-133a is enriched in the heart and dysregulated in heart disease [123]– [128], some changes in gene expression in heart disease may be attributable to changes in miR-133a(v). [score:8]
We used the dual-fluorescence miRNA targeting assay [70] to determine the effects of miR-133a and miR-133a(v) on the expression of a reporter gene with a 3′ gelsolin fragment incorporating the more conserved of the two predicted miR-133a(v) target sites. [score:6]
Complementary pairs of oligonucleotides (25 µM) encoding artificial miRNA sequences (miR-133a canonical isomiR and most common isomiR (miR-133a(v))), a siRNA sequence designed to down regulate mCherry expression (siR-mCh), or a random non -targeting negative control sequence (NTC) were annealed and ligated (T4 DNA ligase; New England Biolabs, Hitchin, UK) into pSM30 restricted with BsmBI (New England Biolabs, Hitchin, UK). [score:6]
Additionally, KCNIP2 (an accessory protein that modulates several cardiac ion channels and is involved in cardiac arrhythmia and heart failure [130]) was downregulated by overexpression of a miR-133a genomic precursor in mouse heart [131]. [score:6]
0065809.g005 Figure 5HEK293 cells were transfected with expression plasmids encoding mCherry with a 3′ partial gelsolin sequence and pSM30 containing inserts for miR-133a, miR-133a(v), a random non -targeting sequence (NTC) or siRNA against mCherry (siR-mCh). [score:5]
HEK293 cells were transfected with expression plasmids encoding mCherry with a 3′ partial gelsolin sequence and pSM30 containing inserts for miR-133a, miR-133a(v), a random non -targeting sequence (NTC) or siRNA against mCherry (siR-mCh). [score:5]
Fig. 5 shows that miR-133a(v) was more effective at suppressing the mCherry-gelsolin construct than was miR-133a, and was comparable to a siRNA targeted against the mCherry sequence. [score:5]
It is plausible that KCNIP2 was downregulated by miR-133a(v) if a substantial proportion of the genomic precursor were processed to form this isomiR. [score:4]
Indeed, DIANA-microT v3.0 (which accepts novel miRNA sequences) [81], [82] predicts 602 target genes for canonical miR-133a and 145 for the 5′ variant (miR-133a(v)), with 90 genes in common. [score:3]
Furthermore there is evidence from miRBase for a similar proportion of miR-133a(v) vs miR-133a expression in human. [score:3]
Differential suppression of a gelsolin sequence-tagged reporter gene by miR-133a isomiRs. [score:3]
This was a surprising finding because KCNIP2 is not a predicted target of miR-133a. [score:3]
Gelsolin is among the 55 genes predicted to be targeted by miR-133a(v) but not by miR-133a itself. [score:3]
A precedent for the possibility of miR-133a isomiR-specific targeting has already been established [61]. [score:3]
Genes predicted by DIANA-microT v3.0 to be targets of miR-133a(v) but not canonical miR-133a include gelsolin and KCNIP2 (KChIP2). [score:3]
miR-22, miR-486, miR133a and miR-143 were detected at greater than 100,000 RPMM. [score:1]
Representative of 3 separate experiments in which miR-133a(v) was significantly more effective than miR-133a. [score:1]
However, miR-378 (Fig. 4G) and the cardiac muscle-enriched miR-133a are exceptions. [score:1]
A good case in point is miR-133a, of which more than half of the reads in our dataset were of a 5′ variant isomiR (miR-133a(v)). [score:1]
Comparison of miR-133a vs miR-133a(v) is indicated (***). [score:1]
As illustrated in Fig. 4C the most frequently recorded miRNA sequence attributed to miR-133a is missing nt no. [score:1]
1; indeed 53.96±0.46% of all miR-133a reads are missing this nt. [score:1]
Number of cells (n): miR-133a 4640; miR-133a(v) 2843; NTC 4088; siR-mCh 3884. [score:1]
[1 to 20 of 24 sentences]
9
[+] score: 70
At the same time, when DNMTs were inhibited, the expression of miR-133a increased, while the expression of CdC42 and RhoA reduced, compared to Phe treated group (Fig. 9D,E). [score:6]
Since CdC42, RhoA and Nelf-A/WHSC2 are the specific target genes of miR-133a 33, we also detected their protein expression levels. [score:5]
These perturbations led to changes of protein synthesis, hypertrophic gene expression and cell size, thereby resulting in cardiac hypertrophy; and 2) Phe might reduce miR-133a expression by increasing the DNA methylation of CpG sites within the miR-133a locus (Fig. 9). [score:5]
At the same time, when miR-133a was overexpressed, the expression of CdC42 and RhoA reduced, compared to Phe treated group (Fig. 10D). [score:4]
As we know, miR-133a is demonstrated to have a critical role in determining cardiomyocyte hypertrophy by regulating its specific target genes: RhoA, CdC42, and Nelf-A/WHSC2 33. [score:4]
DNMTs inhibitor alleviated the enlargement of H9C2 cell size and perturbation of miR-133a, CdC42 and RhoA caused by Phe exposure. [score:3]
Phe increased global DNA methylation, expression of DNMT1, DNMT3a and DNMT3b, and the methylation level of the 5 CpG sites located at the putative transcription start sites of the miR-133a loci in H9C2 cells. [score:3]
The results indicated that Phe might reduce miR-133a expression by increasing DNA methylation of CpG sites within the miR-133a locus. [score:3]
In conclusion, Phe might induce cardiomyocyte hypertrophy through reducing miR-133a expression by DNA methylation, and the following reactivation of CdC42 and RhoA (Fig. 11). [score:3]
In order to further determine the causal role of miR-133a in the enlargement of cell size and perturbations of CdC42 and RhoA, we overexpressed miR-133a in H9C2 cells using miR-133a mimics in the absence or presence of 50 nM Phe. [score:3]
Overexpression of miR-133a alleviated the enlargement of H9C2 cell size and perturbation of CdC42 and RhoA caused by Phe exposure. [score:3]
From our results, Phe exposure reduced miR-133a, which then increased the level of CdC42 and RhoA, and the latter are implicated in the hypertrophic growth response, mediating both morphological changes and the changes in gene expression 44. [score:3]
Over expression of miR-133a. [score:3]
How to cite this article: Huang, L. et al. Phenanthrene exposure induces cardiac hypertrophy via reducing miR-133a expression by DNA methylation. [score:3]
Our results showed that, when miR-133a was overexpressed (Fig. 10A), the cell size reduced compared to the cells treated with Phe only (Fig. 10B,C). [score:2]
As we know, miR-133a is a key regulator in determining cardiomyocyte hypertrophy 33. [score:2]
It is reported that miR-133a can be silenced by DNA hypermethylation 34, and that Phe is capable of increasing DNA hypermethylation through DNMT1 and DNMT3b induction 35. [score:1]
Taking these results together, we think that Phe -induced miR-133a reduction was caused by DNA methylation. [score:1]
We found that Phe exposure significantly reduced the level of miR-133a in H9C2 cells and rat hearts (Figs 4A and 5A). [score:1]
Phe affected miR-133a and transcription factors which are involved in the process of cardiac hypertrophy. [score:1]
Phe induced cardiac hypertrophy through reducing miR-133a, which then increased the level of CdC42 and RhoA. [score:1]
These results indicated that Phe might induce cardiac hypertrophy through reducing miR-133a levels, which then increased the levels of CdC42 and RhoA. [score:1]
To determine the causal role of miR-133a in the enlargement of cell size and perturbations of CdC42 and RhoA, we transfected miR-133a mimics (Qiagen, Venlo, Netherlands) into H9C2 cells in the absence or presence of 50 nM Phe, according to the manufacturer’s instructions. [score:1]
The position of the melting curves indicated that Phe exposure increased the methylation level of the 5 CpG sites located at the putative transcription start sites of the miR-133a loci. [score:1]
Phe reduced miR-133a through increasing DNA methylation. [score:1]
Since the reduction of miR-133a was observed in the present study, we examined whether the Phe -induced miR-133a reduction was caused by DNA methylation, and our results showed that Phe increased global DNA methylation in a dose dependent manner in H9C2 cells. [score:1]
Since reduction of miR-133a was observed in the present study, we further evaluated the global DNA methylation level, the DNA methylation level of CpG sites within the miR-133a locus, and the expression of DNMT1, DNMT3a and DNMT3b. [score:1]
In conclusion, we think that: 1) Phe could induce hypertrophy by perturbing defined miRNAs and transcription factors including miR-133a, CdC42 and RhoA (Fig. 9). [score:1]
Quantification of miR-133a. [score:1]
The position of the melting curves indicated that Phe exposure increased the accumulation of methylation level across the 5 CpG sites located at the putative transcription start sites of the miR-133a loci (Fig. 6E). [score:1]
DNA hypermethylation can silence miR-133a 34, and other research shows that Phe is capable of increasing DNA hypermethylation through DNMT1 and DNMT3b induction 35. [score:1]
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10
[+] score: 64
The miRNA array data have been deposited in the Gene Expression Omnibus (accession number [GEO: GSE22181]) miRNA expression was quantified using real-time RT-PCR on the Applied Biosystems 7500 Real-Time PCR System (Applied Biosystems) to verify the upregulated miRNA targets detected by the miRNA array from the spinal segments (miR-384-3p, miR-325-5p, miR-342-5p, and miR-340-5p) and DRGs (miR-21) in the denervation and sham control groups, and the muscle-specific miRNAs (miR-1, miR-133a, and miR-206) in the soleus muscles of the sham control, entrapment, and decompression groups. [score:10]
In contrast, 3 miRNAs (miR-499, miR-1, miR-133a, and miR-466b) were upregulated in the denervated muscle and 3 miRNAs (miR-329, miR-204, and miR-139-3p) were downregulated after 6 months. [score:7]
The decreased expression of miR-1 and miR-133a was suggested to compensate for the overload by removing the posttranscriptional repression of the necessary target genes [34]. [score:5]
We previously demonstrated that the expression of miR-1 and miR-133 in the soleus muscle of rats increased by ~2-fold at 4 months after sciatic nerve denervation and after reinnervation with microanastomosis [22]; however, the expression of miR-206 was significantly increased by 3-fold at 1 month later and lasted for at least 4 months after reinnervation, but not after denervation [22]. [score:5]
After nerve entrapment using a silastic tube, we observed the downregulation of miR-1 and miR-133a in the soleus muscle at 3 months after its insertion that lasted until at least the 6-months time point (Figure 3). [score:4]
Thus, it is not surprising to discover that the expression patterns of miR-1 and miR-133a were similar. [score:3]
The expression of miR-1 and miR-133a increased in the muscle after 4 months of denervation and reinnervation. [score:3]
Previously, in a rat mo del of sciatic nerve denervation, in the absence or presence of nerve microanastomosis [22], we demonstrated that the expression patterns of miR-1 and miR-133a were similar in the soleus muscle after denervation and reinnervation. [score:3]
Regarding the muscle-specific miRNAs, real-time RT-PCR analysis revealed an ~50% decrease in miR-1 and miR-133a expression levels at 3 and 6 months after entrapment, whereas miR-1 and miR-133a levels were unchanged and were decreased after decompression at 1 and 3 months. [score:3]
After entrapment, the expression of miR-1 and miR-133 was significantly decreased to ~50% of those observed in the sham control group at 3 and 6 months after entrapment. [score:3]
Real-time RT-PCR analysis revealed an ~50% decrease in the expression levels of miR-1 and miR-133a at 3 and 6 months after entrapment, whereas the levels of miR-1 and miR-133a were unchanged and then decreased after decompression for 1 and 3 months, respectively. [score:3]
The expression patterns of miR-1 and miR-133a were similar after entrapment and decompression. [score:3]
In this study, there was an ~50% decrease in the expression levels of miR-1 and miR-133a at 3 and 6 months after entrapment as well as after 1 and 3 months of decompression. [score:3]
It has been reported that the expression of miR-1 and miR-133a decreased during skeletal muscle hypertrophy after 7 days of functional overload in rats. [score:3]
In contrast, the expression pattern of miR-206 was found to be independent from those of miR-1 and miR-133a. [score:3]
After decompression, miR-1 and miR-133a levels were unchanged and sustained a significant decrease at 1 and 3 months later, respectively. [score:1]
miR-1 and miR-133a are transcribed from a common pre-miRNA precursor in the miR-1/miR-133a locus that generates different primary transcripts [33]. [score:1]
Three muscle-specific miRNAs (miR-1, miR-133, and miR-206), with multiple key roles in the control of muscle growth and differentiation, have been the focus of intense research. [score:1]
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11
[+] score: 54
Other miRNAs from this paper: rno-mir-206, rno-mir-1, rno-mir-133b, rno-mir-133c
Since is known that a high expression of miR-133 as well as a SRF reduction repress the expression of MyoD, myogenin and MyHC [40], [54], our results leave us to believe that PRP could be remarkably effective in promoting muscle regeneration by a molecular regulatory mechanism involving also miR-133 -mediated up-regulation of SRF expression levels (Figure 8). [score:11]
We then analyzed, under the same experimental condition, the protein expression of SRF, the most reliable molecular target of miR-133. [score:5]
To understand if the presence of PRP was potentially able to modulate the expression of miRNAs, we analyzed the expression of miR1, miR206 and miR-133a during the early stages of skeletal muscle regeneration. [score:5]
Since myoblast proliferation following myotrauma is orchestrated by multiple factors including growth factors, transcription factors, and miRNAs relating to myogenesis in vivo, in this study we analyzed at 2- and 5-day post-injury the multi-directionally effects of PRP on the expression of several cytokines (TNFα, IL-6, IL-10, IL-1β, and TGF-1β), myogenic response factors (MRFs) (MyoD1, Myf5, Pax7, Myogenin, and Mrf4), GFs (VEGF-A and IGF-1Eb), as well as myo-miRNAs (miR-1, miR-133a, and miR-206), stress-response proteins (Hsp70, Hsp27 and αB-crystallin) and apoptotic markers (NF-κB-p65, Bcl-2, Bax, and caspase 3). [score:4]
In agreement with those data, our results showed that the level of miR-1, miR-206 and miR-133a decreased at day 2 after muscle injury in all experimental groups, returning to pre-injury levels at day 5, with the exception of miR133a, which still remained down-regulated in the presence of PRP. [score:4]
Indeed, an inverse correlation between the expression levels of SRF and miR-133 was observed at least at 5-day post injury when comparing PRP versus NO-PRP or Ctrl samples. [score:3]
The expression pattern of SRF observed in the present study seems to support the hypothesis of a specific effect of PRP on miR-133 function. [score:3]
Real time-PCR analysis of miR-1, miR-133a and miR-206 expression using total RNA isolated from Ctrl-, PRP- and NO-PRP- group at 2 (A) and 5 (B) day post-injury. [score:3]
0102993.g008 Figure 8 The presence of PRP modulated the expression of miR-133a and SRF protein as well as several myogenic response factors such as MyoD1, Pax7, and Myf5, the growth factor IGF-1Eb and both the cytokine IL-1β and TGF-1β. [score:3]
The presence of PRP modulated the expression of miR-133a and SRF protein as well as several myogenic response factors such as MyoD1, Pax7, and Myf5, the growth factor IGF-1Eb and both the cytokine IL-1β and TGF-1β. [score:3]
Differently, it remains controversial whether miR-133 promotes or inhibits muscle cell proliferation [40], [46], [47]. [score:3]
At day 2 after injury, the expression level of miR-1, miR-133a and miR-206 was significantly decreased, more than 0.5-fold with respect to the pre-injured level (p<0.05), independently from the presence or not of PRP (Figure 4A). [score:3]
Among the possible targets of miR133, the most reliable is the serum response factor (SRF), which plays a critical role in muscle proliferation and differentiation depending on its association with co-factors such as myocardin, HOP, and Elk-1 [40], [47], [51]– [53]. [score:3]
Of these, the most wi dely studied are members of miR1, miR206 and miR-133 families [39], [40]. [score:1]
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[+] score: 49
Other miRNAs from this paper: rno-mir-1, rno-mir-133b, rno-mir-133c
miR-1 promotes muscle differentiation by targeting histone deacetylase 4 (HDAC4), a transcriptional repressor of muscle gene expression, and PGC-1alpha (PGC-1α); it also controls the muscle cell phenotype via the regulation of insulin-like growth factor 1 (IGF-1); in contrast, miR-133 modulates muscle proliferation via the repression of serum response factor (SRF)[13, 14]. [score:6]
We therefore analyzed muscle-specific miRNA expression, the expression of miR-1 (an miRNA associated with IGF-1, HDAC4 and PGC-1α in skeletal muscle) and miR-133a/b (SRF -dependent miRNAs). [score:5]
The findings presented here demonstrate that the CIHH rats exhibited a significant reduced running capacity and prominent slow-to-fast muscle fiber shift, which was accompanied by significant increased in miR-1, miR-133 expression and significant reduced in PGC-1α, HDAC4, p-AKT and SRF expression. [score:5]
Analyses of the expression of miR-1, miR-133a and miR-133b were performed by qRT-PCR and normalized to the expression of 5S RNA in the same sample, as described in the Methods section. [score:5]
miR-133 (including miR-133a and miR-133b) regulates muscle proliferation through SRF[13]; thus, we analyzed the expression of SRF in the gastrocnemius via Western blotting (Fig 5). [score:4]
4. Changes in miR-133a/b-related protein expression. [score:3]
Effects of electrical stimulation on the CIHH -induced expression of miR-1, miR-133a and miR-133b. [score:3]
From our study, there is a fact that although miR-133a and miR-133b have very similar sequences[13], they still have distinct functions for muscle specific expression[36]. [score:3]
Electrical stimulation not only prevented the increase in miR-1(p<0.05) but also significantly decreased the miR-133a expression in HE group compared with the HH group (p<0.05). [score:2]
At 2 weeks (Fig 2A), the relative miR-1 and miR-133a expression of the HH group were significantly increased compared with the NC group (p<0.05). [score:2]
It is reasonable to speculate a priority that miR-1 and miR-133 may have roles in the response of CIHH-impaired muscle to changes during electrical stimulation via regulation of related signaling pathways. [score:2]
Four weeks of CIHH exposure (Fig 2B) significantly increased the relative miR-1 (p<0.05) and miR-133a (p<0.05) expression in the HH group compared with the NC group. [score:2]
The HE group exhibited downward trends in the miR-1 and miR-133a expression compared with the HH group; but, these changes were not significant. [score:2]
MyomiRs represent a suite of miRNAs that are highly enriched in cardiac and/or skeletal muscle which including miR-1, miR-133a, miR-133b and so on[12]. [score:1]
miR-1 and miR-133 have distinct roles in the modulation of skeletal muscle proliferation and differentiation[13]. [score:1]
miR-133a may represent a better reflection of CIHH induce rat muscle dysfunction than miR-133b. [score:1]
miR-133 enhances myoblast proliferation by repressing SRF, which is a transcription factor known to block cell proliferation[13]. [score:1]
Interestingly, only miR-133a exhibited a significant increase in the HH group at both 2 and 4 weeks, and partly reversed by 4 weeks electrical stimulation. [score:1]
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13
[+] score: 46
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
MiR-1 and miR-133 have been regarded as key factors involved in cardiac development and cardiovascular disease. [score:4]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
Further pathway analysis indicated that gap junction pathway was the predicted closely correlation pathway to be targeted by miR-1 and miR-133. [score:3]
As shown in Figure 6, the 14 pathways were predicted to be related to the 3 differentially expressed miR-1 and miR-133 family members. [score:3]
It has been reported that Cx43 is a miR-1 and miR-133 target [48, 49], but Cx45 has not been reported yet. [score:3]
The results showed that the expressions of miR-1 and miR-133 were consistent with the microarray data. [score:3]
And WXKL increased the expressions of miR-1 and miR-133 significantly. [score:3]
The relative expressions of miR-1 and miR-133 were validated by quantitative real-time PCR, and the possible effects of WXKL were observed at the same time. [score:3]
Relative Expressions of miR-1 and miR-133. [score:3]
Compared with the control group, the relative expression of miR-133 decreased in the mo del and the captopril groups (P < 0.01 and P < 0.05, resp. [score:2]
Regulatory effects on miR-1, miR-133, Cx43, and Cx45 might be a possible pharmacological mechanism of WXKL in the treatment of MI at the gene level. [score:2]
Compared with the mo del group, the relative expressions of miR-1 and miR-133 increased in the WXKL and the captopril groups (P < 0.01 and P < 0.05, resp. [score:2]
Complex changes of miRNAs and related pathways, including miR-1, miR-133, and gap junction pathway, are involved in the pathogenesis of MI. [score:1]
While the deficiency of miR-133a leads to myocardial matrix remo deling and progress of heart failure [44, 45]. [score:1]
The present study is interested in miR-1 and miR-133, two muscle-enriched miRNAs, and they were chosen for further validation by the quantitative real-time PCR, and the possible effects of WXKL were observed at the same time. [score:1]
MiR-1 and miR-133 are muscle-enriched miRNAs, and they are abundant in the heart. [score:1]
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[+] score: 40
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
In terms of expression patterns within each individual ZT06 group, the 24-hour acute group had a tandem cluster that was differentially expressed, with downregulation of the tumour suppressor miRNAs, miR-1 and miR-133a (Tables 1 and 2). [score:10]
The miR-1/133a cluster has been shown to be downregulated in a variety of cancers, whereas miRNA-133a has also been shown to act as a tumour suppressor in breast cancer cells by causing S/G [2] phase cell-cycle arrest through activity on phosphorylated Akt [28, 29]. [score:6]
In the 24-hour acute ZT06 group, two miRNAs that are part of the same cluster, miR-133a and miR-1, were both underexpressed (Table 2). [score:3]
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15
[+] score: 38
[23] A previous study also suggested that attenuation of miR-1/miR-133 transcription leads to the up-regulation of their direct downstream target cyclin D1,[24] and the abundance of cyclin D1 and expression of miR-17 were inversely correlated. [score:9]
Yu and colleagues revealed that phosphorylated Akt, a downstream target of the phosphatidylinositol-3-kinase (PI3K)/Akt signalling pathway, is up-regulated by decreased miR-1. [21] Similarly, Huang and colleagues found that miR-133 represses the insulin-like growth factor 1 receptor, which is upstream of PI3K/Akt signalling at the post-transcriptional level, and negatively regulates the PI3K/Akt signalling pathway. [score:7]
All miRNAs except miR-17 repress Akt activation, and miR-1 and miR-133 indirectly suppress cyclin D1 expression. [score:6]
miR-1, miR-17, and miR-133 suppress cyclin D expression. [score:5]
A previous study has shown that, of the various miRNAs, the down-regulation of miR-1, miR-133, and miR-17 causes activation of Akt and cyclin D1. [score:4]
Collectively, we conclude that APC and IPC are related to miR-1, miR-17, miR-133, and miR-205, which suppress the Akt–GSK–cyclin D1 pathway. [score:3]
Insulin-like growth factor-1 receptor is regulated by microRNA-133 during skeletal myogenesis. [score:2]
Four miRNAs (miR-1, miR-17, miR-133, and miR-205) related to the Akt–GSK–cyclin D1 pathway were significantly down regulated by both APC and IPC treatment (p < 0.05, Table 2). [score:2]
[1 to 20 of 8 sentences]
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[+] score: 36
Overexpression of miR-133 in cardiomyocytes reduced GLUT4 expression and insulin-stimulated glucose uptake by targeting KLF15. [score:7]
Horie T. Ono K. Nishi H. Iwanaga Y. Nagao K. Kinoshita M. Kuwabara Y. Takanabe R. Hasegawa K. Kita T. MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes Biochem. [score:5]
The expression of miR-133a was persistently increased, and the level of miR-203 was persistently decreased (Figure 4). [score:3]
Therefore, miR-133 may be a potential biomarker to follow the consequences of disease progression at the level of skeletal muscle or cardiac muscles. [score:3]
Overall, a gradual elevation of circulating levels of miR-133a was observed over the disease course. [score:3]
The miR-133a displayed the strongest elevation during disease progression in our study. [score:3]
miR-133a is abundantly expressed in skeletal muscle and myocardial cells [34, 35]. [score:3]
When β cell failure occurred, the circulating level of miR-133a remained high, and additionally, the level of miR-122 was significantly increased, whereas miR-203, miR-450a and miR-434-3p were decreased at this time point (Figure 4). [score:1]
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
Therefore, miR-133 may play an important role in the pathogenesis of insulin resistance in ZDF rats [36]. [score:1]
The highest augmentation of miRNA blood level was observed for miR-133a, which was approximately 28-fold higher at late-stage diabetes than at the pre-diabetes stage (Figure 5). [score:1]
In our study, both the diminution of miR-151-3p and the strong increase in miR-133a level at late-stage diabetes could therefore be the consequence of heart muscle dysfunction. [score:1]
In addition, circulating plasma miR-133a levels are increased in patients with acute myocardial infarction and potentially serve as a marker for cardiomyocyte death [37]. [score:1]
Overall, the blood level of 3 miRNA species is significantly elevated, namely miR-133a, miR-375 and miR-210. [score:1]
Wang F. Long G. Zhao C. Li H. Chaugai S. Wang Y. Chen C. Wang D. W. Plasma microRNA-133a is a new marker for both acute myocardial infarction and underlying coronary artery stenosis J. Transl. [score:1]
Chen J. F. Man del E. M. Thomson J. M. Wu Q. Callis T. E. Hammond S. M. Conlon F. L. Wang D. Z. The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation Nat. [score:1]
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[+] score: 28
Though miR-133 and miR-1 are bicistronic and reported to be jointly regulated during pathological hypertrophy, the expression of miR-1 was downregulated while miR-133 was upregulated in our case (Figs. 2, 4). [score:10]
miR-30 family was downregulated during pathological hypertrophy to activate calcium signaling, apoptosis and autophagy pathways miR-133b CyclinD, Nelf-A, RhoA, Ccd42 The expression of miR-133 was upregulated during physiological cardiac hypertrophy. [score:9]
The expression of miR-133 was upregulated during pathological hypertrophy. [score:6]
A single infusion in vivo of an antagomir oligonucleotide suppressing miR-133 induced a marked and sustained cardiac hypertrophy [29]. [score:3]
[1 to 20 of 4 sentences]
18
[+] score: 28
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
A few notable exceptions are miR-499, an miRNA abundantly expressed in the heart (Figure 2A), which is represented by only one read (Table 2), and the miR-133 family, which is preferentially and abundantly expressed in the heart (Figure 2), and represented by only 7 reads (Table 1). [score:5]
The expression patterns of miR-1 and miR-133 largely overlapped in many tissues examined in this study (Figure 2). [score:3]
These two miRNA genes – miR-1 and miR-133 – exist as a cluster and thus are always expressed together in mouse [42]. [score:3]
Several miRNAs (miR-1, miR-133, miR-499, miR-208, miR-122, miR-194, miR-18, miR-142-3p, miR-101 and miR-143) have distinct tissue-specific expression patterns. [score:3]
Like miR-1, miR-133 is a muscle-specific miRNA (Figure 2) because of its abundant expression in many other muscular tissues such as heart and skeletal muscle [45, 46]. [score:3]
Similarly, we found all members of the miR-15, miR-16, miR-18 and miR-133 families in our sequences, suggesting that all members belonging to these miRNA families are expressed in these three (heart, liver and thymus) tissues. [score:3]
Additionally, miR-1 and miR-133 in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach showed the highest levels of expression. [score:3]
For instance, miR-133 is represented only by 4 clones (two reads each for 133a and 133b) in our sequences, which indicates a 100-fold lower expression level compared with that of miR-1 family, if cloning frequency taken as a measure of expression. [score:2]
The discrepancies between the cloning frequency and small RNA blot results for miRNA-1 and miR-133 could not be attributed to the RNA source because the same RNA samples were used for both experiments (cloning and small RNA blot analysis). [score:1]
We also used approximately a similar amount (activity) of [32]P -labelled probe for detection of miR-1 and miR-133. [score:1]
However, our small RNA blot analysis indicated a different picture as miR-133 was detected as abundantly as miR-1 in the heart (Figure 2). [score:1]
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[+] score: 26
In plasma, miRNA upregulation was observed for miR-133a and miR-133b following PH and SL, whereas miR-100 and miR-466c were similarly downregulated following anesthesia and surgery. [score:7]
Comparing significantly deregulated miRNAs in the SL- and PH-group, we identified 10 miRNAs (rno-miR-100, rno-miR-105, rno-miR-1224, rno-miR-133a/b, rno-miR-383, rno-miR-466c, rno-miR-483, rno-miR-598-5p, and rno-miR-628) that showed similar expression changes in both groups at the same postoperative time point, while one miRNA (rno-miR-29a) was regulated in the opposite direction at the same time point. [score:6]
This notion is further supported by the fact that miR-133a/b are highly expressed in muscle tissue [27, 28] and their increased expression levels in the plasma might likely be the result of muscle trauma during and after laparotomy. [score:5]
Our findings, therefore, suggest that the upregulation of miR-133a/b in plasma samples might be a consequence of surgical stress or trauma rather than being specific to the hepatectomy. [score:4]
The expression of both rno-miR-133a and rno-miR-133b was similarly increased in plasma samples after PH and SL, with a 42-fold (p = 0.04) and 24-fold change (p = 0.01) for miR-133a, respectively. [score:3]
Two of these miRNAs, miR-133a and miR-133b, were also found in our analyses. [score:1]
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20
[+] score: 21
23, 30 However, as miR133a was unchanged in other hypertensive vessels that displayed reduced Kv7.4 expression and miR153 was consistently up-regulated in these vessels, we focused on defining the impact of miR153 on Kv7.4 in hypertension. [score:6]
Synthetic RNA molecules, miR153, miR133a, and non -targeting control (NTC) miR (Active Motif, La Hulpe, Belgium), were designed to mimic endogenous mature miR153, miR133a, or act as a NTC, respectively. [score:3]
[29] In aorta from SHRs, miR133a as well as miR153 increased, but in this artery, the decreased Kv7.4 protein expression was associated with a decrease in mRNA. [score:3]
Interestingly, we reduced KCNQ4 transcript levels in NT MAs by co-transfecting miR153 with miR133a providing support for our hypothesis that in the aorta a rise in miR133a affects KCNQ4 transcription, whereas the rise in miR153 seen in the aorta, renal, and MAs leads to impaired translation of KCNQ4 mRNA. [score:3]
In arteries transfected with miR153, KCNQ4 mRNA expression increased approximately two-fold (N = 4, P = 0.02, Figure  4B), whilst Kv7.4 abundance decreased by 75.43 ± 0.15% (N = 3, P < 0.0001, Figure  4C) compared with NTC miR -transfected vessels, which mirrored the changes recorded for SHRs shown in Figure  1. Cotransfection of NT MAs with miR153 and miR133a showed a marked decrease of KCNQ4 (N = 4, P < 0.05, online, Figure S4 A) but not KCNQ5 (N = 4, P = 0.34, online, Figure S4 B), compared with NTC miR -transfected vessels. [score:1]
This analysis revealed putative seed sequences in KCNQ4 for miR26a, miR214, miR133a, miR200b, miR153, miR218, and let-7d. [score:1]
Twelve-nanomolar miR153 (+ miR133a for cotransfection studies) or NTC miR were transfected into mesenteric or middle cerebral arteries (MCAs) from NT rats using TransIT-X2 and OptiMEM® I Reduced-Serum Medium according to the manufacturer's protocol (Mirus Bio LLC, Madison, USA). [score:1]
In silico analysis of the 3′ UTR of KCNQ4 revealed seed sequences for miR26a, miR133a, miR200b, miR153, miR214, miR218, and let-7d with quantitative polymerase chain reaction showing miR153 increased in those arteries from SHRs that exhibited decreased Kv7.4 levels. [score:1]
A 1.35-fold increase was also observed for miR133a in SHR aorta (N = 6, P = 0.006). [score:1]
Mir133a has been implicated in modulation of the VSMC phenotype in general and specifically in the regulation of VSMC proliferation in mouse aorta. [score:1]
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[+] score: 20
It is noteworthy that miR-1, miR-133, miR-30, miR-208a, miR-208b, mir-499, miR-23a, miR-9 and miR-199a have previously been shown to be functionally involved in cardiovascular diseases such as heart failure and hypertrophy [40], [41], [42], [43], [44], and have been proposed as therapeutic- or disease-related drug targets [45], [46]. [score:7]
In particular, miR-1 and miR-133, which are abundant microRNAs in the heart, are implicated in cardiovascular development and myocardial lineage differentiation, as they tightly control expression of muscle genes and repress ”unwanted” gene transcription through a network of target transcription factors [36], [37], [38], [39]. [score:6]
In particular, several microRNAs that are preferentially expressed in different types of muscles (e. g. miR-1, miR-133, and the myomiRs miR-208, miR-208b and miR-499) play a pivotal role in maintenance of cardiac function [17], [18], and the ablation of microRNAs-RISC machinery can have dramatic effects on cardiac development [19], [20], [21]. [score:4]
An assessment of the degree of conservation for structure-specific distribution of microRNAs in Wistar rat, Beagle dog and cynomolgus monkey (see for relative enrichment analysis), revealed high enrichment of nine microRNAs cardiac valves (miR-let7c, mIR-125b, miR-127, mir-199a-3p, miR204, miR-320, miR-99b, miR-328 and miR-744) (Figure 3A) and seven microRNAs in the myocardium (miR-1, mir-133a, miR-133b, miR-208b, miR-30e, miR-499-5p, miR-30e*) (Figure 3A). [score:1]
Conserved microRNA signatures were identified in valves (miR-let-7c, miR-125b, miR-127, miR-199a-3p, miR-204, miR-320, miR-99b, miR-328 and miR-744) and in ventricular-specific regions of the myocardium (miR-1, miR-133b, miR-133a, miR-208b, miR-30e, miR-499-5p, miR-30e*) of Wistar rat, Beagle dog and cynomolgus monkey. [score:1]
Furthermore, ventricular microRNAs (miR-1, miR-133, miR-208b and miR-499) have been found to be increased in the plasma of patients with myocardial infarction, and might represent a useful alternative to the classical cardiac troponin (cTnI) biomarker [57], [58], [59], [60], [61]. [score:1]
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[+] score: 19
While another group has reported that miR-133a is highly expressed in the sheep heart [17], they did not, as has been done in the present study, specify expression of the different isoforms. [score:5]
Four myocardial-enriched miRNAs, miR-1, miR-133, miR-499 and miR-208, were confirmed to be highly expressed in ovine heart tissue. [score:3]
For the first time we report that not only are the four cardiac-enriched miR-1, miR-133, miR-499 and miR-208 highly expressed in sheep LV, but also provide information on their isomiRs. [score:3]
In this study, NGS detected high counts of oar-miR-133, while array yielded high expression of hsa-/mmu-/rno-miR-133a-3p, which is one nt longer at the 5′ end compared to oar-miR-133. [score:2]
Oar-miR-133 was the main form in sheep heart, while hsa-/mmu-/rno-miR-133a-3p and-5p and hsa-/mmu-/rno-miR-133b were detected at much lower counts. [score:1]
Oar-miR-133 is currently the only cardiac specific miRNA listed in miRBase 21. [score:1]
Of these, oar-miRNA-133 is the only one presently recorded in miRBase (v21). [score:1]
MiR-1, miR-133, miR-499 and miR-208 are highly enriched myocardial miRNAs 27, 28 and are highly conserved across multiple species including human [29], mouse [30] rat [31] and porcine [32]. [score:1]
Cardiac-enriched miR-1-3p, miR-133a-3p, miR-133b-3p, miR-208b-3p and miR-499-3p were screened. [score:1]
The most abundant cardiac-specific miRNA-133 in the sheep heart was oar-miR-133 which has one nt different from hsa-/mmu-/rno-miR-133a-3p (previously hsa-miRNA-133). [score:1]
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23
[+] score: 16
IPA identified 4 focus miRNAs related to metastasis and upper gastrointestinal tract cancer (≥4 fold change) that were downregulated in metastasis positive samples versus metastasis negative samples: 1) miR-92a-3p (p = 0.0001, fold change >14), miR-141-3p (p = 0.0022, fold change >9), miR-451-1a (p = 0.0181, fold change >12) and miR133a-3p (p = 0.0304, fold change >9) (S2 Fig. ). [score:4]
miRNome analysis identified four down-regulated miRNAs in metastasis positive primary tumors compared to metastasis negative tumors: miR-92a-3p (p=0.0001), miR-141-3p (p=0.0022), miR-451-1a (p=0.0181) and miR133a-3p (p=0.0304). [score:3]
Whereas, miR-133b shares sequence homology and gene targets with miR-133a, which was identified as a part of the rat miRNA signature in the present study. [score:3]
al, 3 miRNAs were differentially expressed in human esophageal adenocarcinoma: miR-200a, miR-21, and miR-133a. [score:3]
The 4 miRNAs (miR-92a-3p, miR-451a, miR-141-3p, and miR-133-3p) were significantly down regulated in metastasis positive tumors. [score:2]
The 4 focus miRNAs symbols miR-92a-3p, miR-141-3p, miR-451-1a, and miR133a-3p were mapped from the dataset ID rno-miR-32-5p, rno-miR-141-3p, rno-miR-451-5p, and rno-miR-133b-3p respectively. [score:1]
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24
[+] score: 15
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The expression analysis of selected miRNAs using qRT-PCR also showed that miR-26a and -99a were highly expressed in all tissues, while miR-122 and miR-133a were predominantly expressed in liver and muscle, respectively. [score:7]
Comparison of miRNA expression profiles among tissues revealed that very few miRNAs expression was tissue specific (e. g., miR-9, -124 in brain, miR-122 in liver, miR-1, miR-133a and -206 in muscle). [score:5]
Our comparison of miRNA expression across 11 tissues from bovine revealed a few tissue specific miRNAs: miR-9, -124 in brain, miR-122 in liver, miR-1, miR-133a and -206 in muscle, which had been previously reported in mouse and human [13, 27]. [score:3]
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[+] score: 12
Further, miR-1 enhances cardiomyoblast apoptosis by targeting the expression of Hsp60 and Hsp70, while miR-133 targets and represses caspase-9 expression to decrease cardiomyoblast apoptosis [33]. [score:9]
By contrast, miR-133 promotes the proliferation of myoblasts and inhibits their differentiation [20]. [score:3]
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[+] score: 11
Other miRNAs from this paper: rno-mir-139, rno-mir-1
Similar data were obtained in murine stomach where increase in miRNA-133a was shown to downregulate RhoA and decrease in the smooth muscle contractility [30]. [score:4]
Likewise, studies in rat IAS and mouse stomach have shown that miRNA-133a downregulates RhoA in aging- and diabetes -associated decrease in the respective smooth muscles’ contractility 29, 30. [score:4]
Recent studies from our laboratory have shown that aging leads to changes in certain miRNAs such as miRNA-133a that affect IAS tone by targeting RhoA/ROCK signal transduction cascade critical for the basal IAS tone [29]. [score:3]
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27
[+] score: 11
MiR-499 and miR-21 were downregulated in LPS -induced cells in a dose- and time -dependent manner, while there was no significant change to miR-1, miR-133, and miR-208 expression. [score:6]
In the myocardium of rats with acute myocardial infarction, the expression of some miRNAs was altered, including cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 [15– 17]. [score:3]
Cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 regulate diverse aspects of cardiac function, including cardiomyocyte proliferation, differentiation, contractility, and stress responsiveness. [score:2]
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28
[+] score: 11
Three miRNAs profiles were found with (A) rno-miR-133b-3p, rno-miR-378a-3p, and rno-miR-434-3p equally expressed in both muscle types, (B) rno-miR-1-3p and rno-miR-133a-3p with higher expression in EDL and (C) rno-miR-206-3p, mmu-miR-208b-3p, and rno-miR-499-5p with higher expression in SOL. [score:7]
MicroRNA-1 and microRNA-133a expression are decreased during skeletal muscle hypertrophy. [score:3]
Three miRNAs profiles were found with (A) rno-miR-1-3p and rno-miR-133a-3p rising in response to both SOL and EDL muscle damage, (B) rno-miR-133b-3p, rno-miR-378a-3p, and rno-miR-434-3p with higher levels following EDL muscle damage and (C) rno-miR-206-3p with higher levels following SOL muscle damage. [score:1]
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29
[+] score: 10
For example, rno-miR-1-3p, rno-let-7 family, rno-miR-29a-3p, rno-miR-133a-3p, rno-miR-499-5p and rno-miR-140-3p are most highly expressed in both HF and control group in our study, which was consistent with the previous studies that rno-miR-133, rno-miR-1 and rno-miR-499 are highly expressed in the heart[26], and miR-1, let-7 and miR-133 are highly expressed in the murine heart[27]. [score:7]
The most highly expressed miRNAs were rno-miR-1-3p, rno-let-7 family, rno-miR-29a-3p, rno-miR-133a-3p, rno-miR-499-5p and rno-miR-140-3p in both HF and control group. [score:3]
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30
[+] score: 10
MiR-223 and miR-133 regulate the expression of glucose transporter 4 in cardiomyocytes either by directly targeting GLUT4 3′UTR or indirectly targeting other protein-coding mRNA, e. g., KLF15 [35], [36]. [score:10]
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[+] score: 8
miR-1 promotes myogenesis by targeting histone deacetylase 4 (HDAC4), while miR-133 promotes myoblast proliferation by inhibiting serum response factor (SRF) [57]. [score:5]
Two well-known miRNAs, miR-1 and miR-133, have highly specific expression in cardiac and skeletal muscle tissue [55]. [score:3]
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[+] score: 8
Transgelin 2 (TAGLN2), an inhibitior of cell proliferation in renal carcinoma (RCC), is an intriguing target of miR-133a. [score:5]
TAGLN2 is recognized as an oncogene and diminished expression of miR-133a is frequently shown in RCC [31]. [score:3]
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33
[+] score: 8
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, our data reveal that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p,rno-miR-146a-5p, and rno-miR-1-3p. [score:4]
Picking out 7 miRNAs associated with heart failure and taking statistical analysis, we found that Shenfu injection could significantly downregulate the levels of rno-miR-30c-1-3p, rno-miR-125b-5p, rno-miR-133a-5p, rno-miR-199a-5p, rno-miR-221-3p, rno-miR-146a-5p, and rno-miR-1-3p (Figure 5(b)). [score:4]
[1 to 20 of 2 sentences]
34
[+] score: 8
For example, miR-1 enhances cardiomyocyte apoptosis by regulating the target genes Hsp60 and Hsp70, whereas miR-133 targets and represses caspase-9 expression to decrease cardiomyocyte apoptosis [35]. [score:8]
[1 to 20 of 1 sentences]
35
[+] score: 8
Recently, miR-133 has been the subject of further functional studies, and results have indicated that it is able to inhibit SMC-specific contractile gene expression by directly targeting several smooth muscle mRNAs as well as SRF 33. [score:8]
[1 to 20 of 1 sentences]
36
[+] score: 8
As a parallel control, miR-133 was initially upregulated 12 h after H [2]O [2] and downregulated 48 h after H [2]O [2] (Figure 2d). [score:7]
miR-133 was used as a negative control. [score:1]
[1 to 20 of 2 sentences]
37
[+] score: 8
Studies also showed that miR-21 [26], miR-26 [27], miR-328 [28], miR-133 and miR-590 [29] participated in the process of AF by controlling the expression of their specific gene targets. [score:5]
Overexpression of miR-133 or miR-101 attenuated cardiac hypertrophy [20] or cardiac fibrosis [21] respectively. [score:3]
[1 to 20 of 2 sentences]
38
[+] score: 7
The most up-regulated were circRNA_008964, miR-133a-5p, and BGLAP with FCs of 16.97, 355.67, and 22.96, respectively, whereas circRNA_017759, miR-551b-3p, and IL-1RN were the most down-regulated, with corresponding FCs of 6.32, 257.63 and 14.21. [score:7]
[1 to 20 of 1 sentences]
39
[+] score: 7
By comparing the venous plasma microRNA expression profiles from patients with Takotsubo cardiomyopathy or acute myocardial infarction, miR-16 and miR-26a were found to be highly expressed in Takotsubo cardiomyopathy patients, while miR-1 and miR-133a were highly expressed in acute myocardial infarction patients. [score:7]
[1 to 20 of 1 sentences]
40
[+] score: 7
qPCR of left atrial chambers demonstrated that miR-1, miR-26b, miR-29a, miR-30e, miR-106b, miR-133 and miR-200 are up-regulated in HTD rats as compared to controls (Fig 1), demonstrating a similar microRNA expression profile as in atrial-specific Pitx2 deficient mice [14, 16]. [score:5]
Several lines of evidence have already reported the key regulatory role of miR-1 [60– 62], miR-26 [63], miR-106b [64], miR-133 [65– 66] and miR-200 [64] in arrhythmogenesis. [score:2]
[1 to 20 of 2 sentences]
41
[+] score: 7
Moreover, the microRNAs miR-103, miR-107, miR-133a, miR-145, mir146a and miR-98, which presented altered expression at 7 days after SCI in both Liu's study [6] and ours, demonstrated significant alterations in the expression of their targets, according to De Biase et al. [7]. [score:7]
[1 to 20 of 1 sentences]
42
[+] score: 6
MicroRNA-1 and microRNA-133a expression are decreased during skeletal muscle hypertrophy. [score:3]
miR that regulate targets in the mTORC1 pathway (hsa-miR-16-5p, hsa-miR-26b-5p, hsa-miR-99a-5p, hsa-miR-100-5p, hsa-miR-128a-3p, hsa-miR-133a-3p, hsa-miR-199a-3p, hsa-miR-221-3p) were analyzed using TaqMan® microRNA Assays (Applied Biosystems, Foster City, CA, USA). [score:3]
[1 to 20 of 2 sentences]
43
[+] score: 6
Intriguingly, MAPKs are known regulators of miR-1/miR-133 biogenesis [52] and we have recently shown in vascular smooth muscle cell that ERK1/2 activation suppresses miR-133 expression [13], the miR-1 cognate bicistronic gene. [score:6]
[1 to 20 of 1 sentences]
44
[+] score: 6
There were no significant changes in the expression of miR-15, miR-30, and miR-133a between healthy subjects and patients with burn injury. [score:3]
We assessed the levels of let-7b, let-7e, miR-194, miR-15, miR-133a, miR-15, and miR-195 (as a non-specific control) by real-time PCR. [score:1]
MiR-195, let-7e, miR-15, miR-133a, and miR-30 did not show any significant difference between burn rats and sham rats (Figure 1A) (P>0.05). [score:1]
MiR-15, miR-133a, and miR-30 also had P [CT] > 0.75. [score:1]
[1 to 20 of 4 sentences]
45
[+] score: 6
For example, previous published studies showed that inhibition of miR-1 [29], miR-23a [30], or miR-133 [31] expression accelerated cardiaomyocyte hypertrophy, while other studies demonstrated that myocardial hypertrophy was regulated by miR-22 and miR-30a in vivo and in vitro [32], [33]. [score:6]
[1 to 20 of 1 sentences]
46
[+] score: 6
Despite tissue- and pathology-specificity of miRNAs expression, we failed to identify miRNAs, such as miR-133a and miR-423-5p, as circulating prognostic biomarkers of cardiac remo delling post-MI [14]. [score:3]
Among the 11 miRNAs quantified, 4 were not modulated after 7 days or 2 months MI: miR-29b-3p, miR-338-3p, miR-133a and miR-483-3p interacting respectively with tropomyosin alpha-1 chain, pyruvate kinase PKM and phosphoglycerate mutase 1 (Fig.   1B–E). [score:1]
Up to now, we failed to identify miRNAs, such as miR-133a and miR-423-5p, as circulating prognostic biomarkers of cardiac remo delling post-MI [14]. [score:1]
Bauters C Circulating miR-133a and miR-423-5p fail as biomarkers for left ventricular remo deling after myocardial infarctionInt. [score:1]
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47
[+] score: 6
miRNAs such as miR-133a, miR-185, miR-152, miR-34a and miR-342 which were reported to show increased expression were also up-regulated in our rat mo del. [score:6]
[1 to 20 of 1 sentences]
48
[+] score: 5
ERK1/2 regulation of miRNAs has been previously addressed as it modulated the expression of miR-133a in cardiac myocytes [25], and miR-145 in vascular smooth muscle cells [26]. [score:4]
miR-133a and miR133b are implicated in cardioprotection during ischemic postconditioning [12], and remote ischemic preconditioning [13]. [score:1]
[1 to 20 of 2 sentences]
49
[+] score: 5
For example, mir-133 and mir-30d have been documented to directly downregulate connective tissue growth factor and may be potential therapeutic strategies for the prevention of the progression of structural changes in the extracellular matrix of myocardial cells. [score:5]
[1 to 20 of 1 sentences]
50
[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
[1 to 20 of 1 sentences]
51
[+] score: 5
MicroRNAs have been proved to be potential biomarkers for ischemic heart disease, such as mir-1, mir-133, mir-208, and mir-499 [4– 6]. [score:3]
Tanshinone IIA, a lipid-soluble pharmacologically active compound extracted from the rhizome of traditional Chinese herb Salvia miltiorrhiza, has been reported to improve hypoxic cardiac myocytes and postinfarction rat cardiomyocytes by regulating mir-133 and mir-1 and MAPK pathways [21, 22]. [score:2]
[1 to 20 of 2 sentences]
52
[+] score: 5
Kuwabara Y. Ono K. Horie T. Nishi H. Nagao K. Kinoshita M. Watanabe S. Baba O. Kojima Y. Shizuta S. Increased microRNA-1 and microRNA-133a levels in serum of patients with cardiovascular disease indicate myocardial damage Circ. [score:3]
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of microRNAs in myocardial matrix remo deling Circ. [score:2]
[1 to 20 of 2 sentences]
53
[+] score: 5
Taken together, we identified miR-133 as a novel suppressor of CCL2 in chondrocytes. [score:3]
In the present study, we predicted and selected out the potential miRNAs of CCL2 by choosing the conserved ones, miR-124 and miR-133. [score:1]
The high-throughput screening technology should be used to select out those functional miRNAs besides miR-124 and miR-133 in the future. [score:1]
[1 to 20 of 3 sentences]
54
[+] score: 5
Notably, a panel of 11 Runx2 -targeting miRNAs (miR-23a, miR-30c, miR-34c, miR-133a, miR-135a, miR-137, miR-204, miR-205, miR-217, miR-218, and miR-338) is expressed in a lineage-related pattern in mesenchymal cell types [20]. [score:5]
[1 to 20 of 1 sentences]
55
[+] score: 5
Many miRNAs are expressed in a tissue-specific manner, such as cardiac and skeletal-specific miRNAs (miR-1, miR-133, miR-206), which have been shown to regulate muscle development and function 34 35. [score:5]
[1 to 20 of 1 sentences]
56
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Cesana et al. showed that a long-intergenic ncRNA (lincRNA), linc-MD1, regulates muscle differentiation by interacting with two miRNAs, miR-135 and miR-133, which can bind to MAML1 and MEF2C to regulate their expression levels. [score:5]
[1 to 20 of 1 sentences]
57
[+] score: 4
Gain- and loss-of-function miRNA studies and luciferase reporter assays reported that miR-204 [24], miR-133a [25], and miR-30b-c [26] inhibited the osteogenic differentiation of mice VSMCs and human coronary artery smooth muscle cells (SMCs) during β-glycerophosphate -induced calcification through the targeting of RUNX2. [score:4]
[1 to 20 of 1 sentences]
58
[+] score: 4
MiR-133a protects the heart from pressure-overload induced injury by inhibiting the expression of β [1]-Ars [17]. [score:4]
[1 to 20 of 1 sentences]
59
[+] score: 4
For example, mir-503 was found markedly reduced while mir-133a was found significantly upregulated in peripheral blood mononuclear cells of postmenopausal osteoporosis patients, respectively [12, 13]. [score:4]
[1 to 20 of 1 sentences]
60
[+] score: 4
Other miRNAs from this paper: rno-mir-133b, rno-mir-133c
It has been discovered that Klf4 plays a critical role in the phenotypic transitions of VSMCs that have favorable effects in inhibiting plaque pathogenesis [13]; and a microRNA gene (miR-133) also appears to be a key regulator of VSMCs phenotypic switch in vitro and in vivo [32]. [score:4]
[1 to 20 of 1 sentences]
61
[+] score: 4
MiR-1 and miR-133 were down-regulated in exercised trained rats and cardiac-specific Akt transgenic mice 11, 12. [score:4]
[1 to 20 of 1 sentences]
62
[+] score: 4
Other miRNAs from this paper: rno-mir-133b, rno-mir-499, rno-mir-133c
Cardiac microRNA-133 is down-regulated in thyroid hormone -mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor. [score:4]
[1 to 20 of 1 sentences]
63
[+] score: 4
Moreover, the up-regulation of miR-133 could stimulate GnRH and further impact FSH release [10]. [score:4]
[1 to 20 of 1 sentences]
64
[+] score: 4
Interestingly, the miR-133 family, together with miR-1, miR-206 and miR-208, is specifically expressed in muscle; thus, these miRNAs are called myomiRs 42. [score:3]
Moreover, miR-133a, which differs from miR-133b by only one nucleotide, is crucial for early embryonic survival 43. [score:1]
[1 to 20 of 2 sentences]
65
[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-1, rno-mir-133b, rno-mir-133c
The role of miRNAs in IPostC was further demonstrated in a study by He et al. [11], which showed the upregulation of miR-1 and miR-133 by IPostC during reperfusion in a rat mo del. [score:4]
[1 to 20 of 1 sentences]
66
[+] score: 3
Duisters RF, Tijsen AJ, Schroen B, Leenders JJ, Lentink V, van der Made I, et al. miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
miR-133a was chosen because of its known involvement in controlling the phenotypic switch in vascular smooth muscle cells [22, 23]. [score:1]
[1 to 20 of 2 sentences]
67
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
For example, miR-1 and miR-133 are specifically expressed in muscles. [score:3]
[1 to 20 of 1 sentences]
68
[+] score: 3
It is reported that miR-133a suppresses Smad3/4 -mediated TGF-β signaling [17]. [score:3]
[1 to 20 of 1 sentences]
69
[+] score: 3
The expression of mir-29b and mir-133 in the heart has been confirmed by northern blot [19]. [score:3]
[1 to 20 of 1 sentences]
70
[+] score: 3
6 was illustrated in Fig.   8B, including rno-mir-207, rno-mir-152, rno-mir-133a, may repress the expression of negative modulators, for example, Fads6, Samd14 and Fbxo46, respectively. [score:3]
[1 to 20 of 1 sentences]
71
[+] score: 3
MiR-29, miR-133 and miR-30c are the most strongly fibrosis -associated miRNAs targeting a number of extracellular-matrix-related mRNAs [31], [32]. [score:3]
[1 to 20 of 1 sentences]
72
[+] score: 3
Microarray analysis identified a panel of miRNAs, which are either highly expressed in the heart (miR-1, miR-133a and miR-16) or in the liver (miR-122, miR-192 and miR-194) or invariant (miR-21; Supplementary Figure 1a). [score:3]
[1 to 20 of 1 sentences]
73
[+] score: 3
From 30 selected miRNAs, 6 miRNAs were found altered within muscle tissue after exercise, while just 2 circulating miRNAs (miR-133a, miR-149) were found increased 4 h after exercise (Orton et al., 2005). [score:1]
Circulating miR-1, miR-133a, and miR-206 levels are increased after a half-marathon run. [score:1]
Cycling acute or chronic exercise did not change the serum levels of muscle-enriched miRNAs (miR-1, miR-133a, miR-133b, miR-206, miR-208b, miR-486, and miR-499) with an exception for miR-486, which showed a significant negative correlation with VO [2max] (Pedersen et al., 2007). [score:1]
[1 to 20 of 3 sentences]
74
[+] score: 2
It has been observed that many miRNAs regulate cell apoptosis, such as miR-1, miR-133, miR-199, miR-208, miR-320, miR-21, and miR-204, etc [18- 23]. [score:2]
[1 to 20 of 1 sentences]
75
[+] score: 2
miR-133 protects the heart from apoptosis through direct repression of multiple key components along β1-adrenergic receptor signal transduction, such as adbr1, adcy6, prkacb, and epac [10]. [score:2]
[1 to 20 of 1 sentences]
76
[+] score: 2
Linc-MD1 is required for appropriate muscle differentiation, at least in part because it regulates the levels of myocyte enhancer factor 2C (MEF2C) and mastermind-like protein 1 (MAML1) by sponging endogenous miR-133 and miR-135 in the cytoplasm of muscle cells [24]. [score:2]
[1 to 20 of 1 sentences]
77
[+] score: 2
Other miRNAs from this paper: rno-mir-148b, rno-mir-21, rno-mir-25, rno-mir-26a, rno-mir-148a
b RT-qPCR results of miR-21, miR-25, miR-26a, miR-133a and miR-148 in plasma from 35 indifferent control, 35 LRI control and 70 wheezing + LRI children. [score:1]
In a set of wheezing + LRI patients (n = 20) and age- and gender-matched LRI control children (n = 20), miR-21, miR-25, miR-26a, miR-133a and miR-148 showed potential statistical differences between the patient and control groups (p < 0.10) (Fig.   1a). [score:1]
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78
[+] score: 2
J Cereb Blood Flow Metab 79 Duisters RF Tijsen AJ Schroen B Leenders JJ Lentink V 2009 miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
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79
[+] score: 2
Liu et al. discovered that, as a downstream gene of fibrotic TGF-β/Smad3 pathway, miR-133 can negatively regulate TGF-β/Smad3 [35]. [score:2]
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80
[+] score: 2
The lncRNA linc-MD1 competes with miR-133 and miR-135 to regulate myoblast differentiation [55]. [score:2]
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81
[+] score: 2
The miRNAs miR-29 family and miR-133 regulate mRNAs that encode proteins involved in fibrosis during the pathologic cardiac remo deling [32, 33]; however, the participation of these miRNAs in physiologic cardiac remo deling induced by pregnancy is still unknown. [score:2]
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82
[+] score: 2
Xu et al. found that the muscle-specific miRNAs, miR-1 and miR-133, regulated myocardial apoptosis in an opposing action, with miR-1 being pro-apoptotic and miR-133 being anti-apoptotic [12]. [score:2]
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83
[+] score: 1
A few miRNAs are found to be enriched in the heart including miR-1, miR-133, miR-208a, miR-208b, and miR-499. [score:1]
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84
[+] score: 1
Other miRNAs from this paper: rno-mir-133b, rno-mir-133c
MiR-133 promotes cardiac reprogramming by directly repressing Snai1 and silencing fibroblast signatures. [score:1]
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85
[+] score: 1
It has also been reported that plasma levels of some miRNAs (mir-1, mir-208, mir-133a, mir-423-5p, mir-499) can be used as biomarkers for myocardial injury [90– 92]. [score:1]
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86
[+] score: 1
Among them, five miRNAs (let-7b, miR-1180, miR-183, miR-550b, and miR-133a) were only present in LPS pre-Exo. [score:1]
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87
[+] score: 1
Likewise, a combination of miR-1, miR-133, miR-208 and miR-499 is capable of reprogramming fibroblasts into cardiomyocytes [21]. [score:1]
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88
[+] score: 1
Chen J. F. Man del E. M. Thomson J. M. Wu Q. Callis T. E. Hammond S. M. Conlon F. L. Wang D. Z. The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation Nat. [score:1]
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89
[+] score: 1
For example, miRNAs involved in cardiac hypertrophy and heart failure such as miR-208, miR-133, miR-195, miR-21, and miR-126 have been reported in several studies [5- 8]. [score:1]
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90
[+] score: 1
In our study, we found that several possible interacting pathways among ceRNAs exist, including the following: MRAK161211, MRAK150340/miR-219b/mRNAs (e. g., Tollip, and Ubqln4); XR_006440/miR-365, let7/mRNAs (e. g., Usp31, Usp42, Clcn4–2); and MRAK161211/miR-133/Usp13. [score:1]
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91
[+] score: 1
Dozens of miRNAs have been identified in myocardial cells, including miR-133a, miR-133b, miR-1d, miR-296, miR-21, miR-208 and miR-195 (4– 18). [score:1]
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92
[+] score: 1
Furthermore, many miRNAs have been reported to play a role in diabetic heart, such as miR-1 [9], miR-133a [10], and miR-320 [11]. [score:1]
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93
[+] score: 1
Similarly, miR-1 and miR-133, known to have alternative effects on oxidative stress -induced apoptosis in myocytes [35], the former being pro-apoptotic and the latter anti-apoptotic, were not altered in the present study. [score:1]
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94
[+] score: 1
The canonical myomirRs are miR-1, miR-133a/b, and miR-206. [score:1]
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95
[+] score: 1
In 2014, miR-1, miR-133a, miR-133b, and miR-206 were validated as muscle-specific miRNAs in rat [30]. [score:1]
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96
[+] score: 1
Therefore, the absence of miR-145 and other muscle-specific miRNAs, that is, miR-133a and miR-133b, might clarify kidney injury. [score:1]
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97
[+] score: 1
B) Quantitative relative real-time PCR of miR- miR-133, 19a, miR-34a, miR-326 and miR-193a. [score:1]
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98
[+] score: 1
Clinical chemistry parameters including amylase and lipase (markers of pancreas injury), miR-122-5p (liver enriched), miR-133a-3p (muscle enriched), 148a-3p (pancreas enriched), 208a-3p (heart enriched) and pancreas miRNAs conserved between rat and dog (Table  2) were examined for changes in the serum. [score:1]
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