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61 publications mentioning rno-mir-133c

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

1
[+] score: 188
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]
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]
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]
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]
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]
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]
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]
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]
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]
b Fluorescence image of GFP [+] 293NT infected with lentivirus carrying pre-miR-133. [score:1]
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2
[+] score: 45
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]
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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3
[+] 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]
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4
[+] score: 29
Other miRNAs from this paper: rno-mir-133a, rno-mir-206, rno-mir-1, rno-mir-133b
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]
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]
Differently, it remains controversial whether miR-133 promotes or inhibits muscle cell proliferation [40], [46], [47]. [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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5
[+] 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]
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6
[+] 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-133a, 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, 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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7
[+] score: 19
Other miRNAs from this paper: rno-mir-133a, rno-mir-1, rno-mir-133b
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]
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]
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]
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]
miR-1 and miR-133 have distinct roles in the modulation of skeletal muscle proliferation and differentiation[13]. [score:1]
miR-133 enhances myoblast proliferation by repressing SRF, which is a transcription factor known to block cell proliferation[13]. [score:1]
[1 to 20 of 6 sentences]
8
[+] score: 18
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]
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]
[1 to 20 of 4 sentences]
9
[+] score: 17
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]
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]
Therefore, miR-133 may play an important role in the pathogenesis of insulin resistance in ZDF rats [36]. [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]
[1 to 20 of 5 sentences]
10
[+] score: 13
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 is currently the only cardiac specific miRNA listed in miRBase 21. [score:1]
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]
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]
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]
[1 to 20 of 8 sentences]
11
[+] 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]
[1 to 20 of 2 sentences]
12
[+] score: 11
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]
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]
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 3 sentences]
13
[+] 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]
[1 to 20 of 3 sentences]
14
[+] 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]
[1 to 20 of 1 sentences]
15
[+] score: 10
Other miRNAs from this paper: rno-mir-133a, rno-mir-133b
Furthermore, miR-133 expression was also negatively regulated by the ERK1/2 signaling pathway. [score:4]
In their study, downregulation of ERK1/2 phosphorylation by miR-133 was detected. [score:4]
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]
[1 to 20 of 3 sentences]
16
[+] score: 9
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 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]
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]
[1 to 20 of 3 sentences]
17
[+] 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]
[1 to 20 of 2 sentences]
18
[+] 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]
19
[+] score: 8
It was reported that miR-133 exhibited an anti-apoptotic effect in IR by regulating the expression of CASP9 [15]. [score:4]
Among the miRNAs, miR-1 and miR-133 are specifically expressed in cardiac and skeletal muscles [14, 15]. [score:3]
MiR-1 and miR-133 produced opposing effects on apoptosis induced by H [2]O [2 ][15]. [score:1]
[1 to 20 of 3 sentences]
20
[+] 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]
21
[+] 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]
22
[+] 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]
23
[+] score: 7
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]
[1 to 20 of 1 sentences]
24
[+] 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]
25
[+] 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]
26
[+] 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]
27
[+] score: 5
Other miRNAs from this paper: rno-mir-133a, rno-mir-1, rno-mir-133b
Similarly, it was reported that miR-133 targeted SIRT1 in glioma cells, leading to inhibition of cell proliferation [50]. [score:5]
[1 to 20 of 1 sentences]
28
[+] 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]
29
[+] 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]
30
[+] 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]
31
[+] 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]
32
[+] 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-133a, 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-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]
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33
[+] 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]
34
[+] score: 4
Other miRNAs from this paper: rno-mir-133a, rno-mir-133b, rno-mir-499
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]
35
[+] 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]
36
[+] score: 4
Other miRNAs from this paper: rno-mir-133a, rno-mir-133b
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]
37
[+] 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]
38
[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-133a, rno-mir-1, rno-mir-133b
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]
39
[+] 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-133a, 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, 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]
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40
[+] score: 3
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]
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41
[+] 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]
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42
[+] score: 3
The expression of mir-29b and mir-133 in the heart has been confirmed by northern blot [19]. [score:3]
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43
[+] 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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44
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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]
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45
[+] 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]
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46
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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]
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47
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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]
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48
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The lncRNA linc-MD1 competes with miR-133 and miR-135 to regulate myoblast differentiation [55]. [score:2]
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49
[+] score: 2
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]
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50
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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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51
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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]
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52
[+] 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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53
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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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54
[+] 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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55
[+] 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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56
[+] 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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57
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Other miRNAs from this paper: rno-mir-133a, rno-mir-133b
MiR-133 promotes cardiac reprogramming by directly repressing Snai1 and silencing fibroblast signatures. [score:1]
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58
[+] 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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59
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B) Quantitative relative real-time PCR of miR- miR-133, 19a, miR-34a, miR-326 and miR-193a. [score:1]
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60
[+] 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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61
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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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