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49 publications mentioning rno-mir-195

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-195. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 208
Overexpression of miR-195 in HSC-T6 suppressed Smad7 expression and upregulated α-SMA expression induced by TGF- β [1], and inhibition of miR-195 suppressed α-SMA expression and increased Smad7 expression induced by TGF- β [1]. [score:20]
Our research showed that miR-195 inhibitor did not reduce the level of α-SMA or elevate the level of Smad7 at 72 h, we conclude that miR-195 inhibitor could not regulate the α-SMA and Smad7 expression with a time -dependent manner, on one aspect, the transfection reagents play the best effect at different time in different cells, and on the other aspect, TGF- β [1] could significantly reduce the Smad7 level and increase α-SMA level at a time -dependent manner which may counteract the transfection reagents role in 72 h. To determine whether Smad7 was the target of miR-195, the 3′UTR of the Smad7 mRNA target region was cloned into the pMIR-REPORT luciferase plasmid, and the construct was cotransfected into HEK 293T cells, along with the miR-195 precursor or miR-NC (Figures 6(a) and 6(b)). [score:12]
The miR-195 inhibitors blocked the activation of HSCs, reduced the expression of miR-195 and α-SMA (P < 0.01), and upregulated the expression of Smad7 (P < 0.05). [score:10]
MiR-195 Promotes HSC Proliferation and Modulates TGF- β [1]-Mediated α-SMA and Smad7 ExpressionTo further establish the potential role of miR-195 in HSC activation, HSC-T6 was treated with miR-195 mimics (25 nM, 50 nM, and 100 nM), miR-195 mimic controls, miR-195 inhibitors (50 nM, 100 nM, and 200 nM), and miR-195 inhibitor controls for 24 h, and qRT-PCR was used to measure miR-195 expression. [score:7]
With regard to HSCs, Sekiya found that, during primary HSCs (pHSCs) activation, miR-195 was downregulated on the 10th day compared with the 1st day, and miR-195 could decrease cyclin E expression and inhibit cell proliferation induced by interferon-B [21]. [score:7]
The miR-195 mimic could decrease Smad7 mRNA at 24 h, 48 h, and 72 h and decrease protein expression compared with the TGF- β [1] group at 24 h; at the same time, the miR-195 inhibitor could increase Smad7 mRNA at 24 h and 48 h and increase Smad7 protein expression in comparison with the TGF- β [1] group (Figures 5(c) and 5(d)). [score:6]
In HCC, miR-195 inhibited the cell cycle by downregulating cell cycle protein D, the transcription factor E2F3, and cyclin -dependent kinase 6 [18– 20]. [score:6]
HSC-T6 was treated with TGF- β [1] and miR-195 mimic or miR-195 inhibitor, and we examined their effects on miR-195, α-SMA, and Smad7 expression. [score:5]
To further establish the potential role of miR-195 in HSC activation, HSC-T6 was treated with miR-195 mimics (25 nM, 50 nM, and 100 nM), miR-195 mimic controls, miR-195 inhibitors (50 nM, 100 nM, and 200 nM), and miR-195 inhibitor controls for 24 h, and qRT-PCR was used to measure miR-195 expression. [score:5]
MicroRNA target prediction analyses indicated that miR-195 could target the 3′UTR region of Smad7. [score:5]
The following day, the medium was replaced with Opti-MEM (Invitrogen, USA), and the cells were transfected with an miR-195 inhibitor (200 nM) and miRNA inhibitor control (200 nM) (RiboBio, China) using the transfection reagent siRNA-Mate (GenePharma, China) for 24 h. After 24 h of transfection, the medium was replaced with DMEM containing 10% FBS, and TGF- β [1] was added at a concentration of 5 ng/ml. [score:5]
Figure 2(b) shows that TGF- β [1] increased miR-195 expression at 5 ng/mL and 10 ng/mL, TGF- β [1] significantly increased miR-195 expression, and there were no differences between them. [score:5]
MicroRNA target prediction analysis indicated that miR-195 can target the 3′UTR region of Smad7. [score:5]
Previous studies showed that miR-195 could bind to Smad7 and its target site was located within 1611 and 1630 nt of Smad7 mRNA 3′-UTR and miR-195 was possibly a tumor promoter in U87 cells by targeting Smad7 [22, 28]. [score:5]
Our study showed that miR-195 expression was upregulated in liver fibrotic tissues compared with the control tissues in vivo. [score:5]
Cells were seeded in a 96-well plate at a density of 1 × 10 [3] cells per well and treated with 1, 2, 4, 6, and 8 ng/mL TGF- β1 for 24 h, 48 h, and 72 h. HSC-T6 cells were transfected with miR-195 mimics, miR-195 mimic controls, miR-195 inhibitors, and miR-195 inhibitor controls as described above. [score:5]
The results confirmed that Smad7 was a target of miR-195, and miR-195 bound directly to the 3′UTR region of Smad7 mRNA. [score:4]
All miR-195 mimic, mimic controls, inhibitor, inhibitor control, and primers for miRNA PCR were purchased from RiboBio (Guangzhou, China). [score:4]
Duan and Chen demonstrated that miR-195 was upregulated by TGF- β1 in a dose -dependent manner enhancing glioma cell invasion and proliferation in U87 cells [22]. [score:4]
Furthermore, miR-195 activated HSCs through direct targeting of Smad7. [score:4]
Other studies showed that miRNA-195 was upregulated in hexahydro-1,3,5-trinitro-1,3,5-triazine- (RDX-) treated rats with liver fibrosis [14]. [score:4]
These findings collectively indicated that Smad7 was a direct target of miR-195. [score:4]
Enhanced α-SMA mRNA induced by TGF- β [1] was significantly decreased in the presence of the miR-195 inhibitor at 24 h and 48 h and the miR-195 mimic could increase the α-SMA mRNA expression compared with the TGF- β [1] group at 24 h, 48 h, and 72 h (Figure 5(b)). [score:4]
Thus, our study aimed to determine whether miR-195 regulated HSC activation and Smad7 expression. [score:4]
Other studies showed that miR-195 could bind to Smad7 and regulate Smad7 expression in U87 cells and Caco-2 cells [22, 28]. [score:4]
Collectively, we demonstrated that miRNA-195 activated HSCs by targeting Smad7. [score:3]
These findings indicate that miR-195 is a potential biomarker of hepatic pathogenesis and a possible therapeutic agent for treating liver diseases. [score:3]
Identification of miR-195 as a novel marker involved in HSC activation and liver fibrosis supports its potential utility as a therapeutic target. [score:3]
Growing evidence has demonstrated that miR-195 plays an important role in the neoplastic disease; however, studies on the relationship between miR-195 and liver fibrosis are far from enough. [score:3]
The data showed that 100 nM of the miR-195 mimic significantly increased the miR-195 level in HSC-T6, and 200 nM of the miR-195 inhibitor significantly reduced the miR-195 level in HSC-T6 (Figures 4(a) and 4(b)). [score:3]
In conclusion, our study provides new clues for the role of miR-195 in HSCs activation, and our results demonstrated that miR-195 activates HSCs by targeting Smad7 and promoting HSCs activation and proliferation. [score:3]
The expression levels of miR-195, Smad7, and α-SMA in HSC-T6 transfected, respectively, with miR-195 mimic, inhibitor, or control were measured by qRT-PCR. [score:3]
Smad7 Was the Target of miR-195. [score:3]
We select a concentration of 5 ng/ml for TGF- β [1], because TGF- β [1] at a concentration of 5 ng/ml and 10 ng/ml could both significantly increase miR-195 expression and there were no differences between them. [score:3]
These results suggested that miR-195 induced α-SMA expression in activated HSCs. [score:3]
Then, HSC-T6 was treated with different concentrations of TGF- β [1] (2 ng/mL, 5 ng/mL, and 10 ng/mL) for 24 h to detect the miRNA-195 expression. [score:3]
Dual luciferase reporter assays were performed to verify that Smad7 was the target of miRNA-195. [score:2]
Dual luciferase reporter assays showed that the miR-195 mimic significantly suppressed the luciferase activity of a reporter plasmid carrying the binding site of miR-195 on the 3′UTR of Smad7 (P < 0.05). [score:2]
MiR-195 Promotes HSC Proliferation and Modulates TGF- β [1]-Mediated α-SMA and Smad7 Expression. [score:2]
HSC-T6 was treated with 5 ng/mL TGF- β [1] for 24 h, 48 h, and 72 h, and qRT-PCR showed that TGF- β [1] significantly increased α-SMA and miR-195 expression compared to the control group at 24 h, 48 h, and 72 h (P < 0.01) (Figures 3(a) and 3(c)). [score:2]
MiR-195 plays various roles in different diseases. [score:2]
MiR-195, an important member of the miR-15 family, plays a crucial role in regulating cell cycle progression and cell apoptosis [15]. [score:2]
Enhanced miR-195 induced by TGF- β [1] was significantly decreased in the presence of the miR-195 inhibitor, and the miR-195 mimic could increase the miR-195 level compared with the TGF- β [1] group at 24 h, 48 h, and 72 h (Figure 5(a)). [score:2]
Cells were additionally transfected with miR-195 mimics (100 nM) and miRNA mimic controls (200 nM) using siRNA-Mate for 24 h. Total RNA was extracted from HSC-T6 cells with TRIzol (OMEGA, CA, USA) and a miRNeasy Mini kit (Toyobo, Osaka, Japan). [score:1]
However, the precise roles of miR-195 in the TGF- β [1]/Smad pathway in HSCs remain unclear to date. [score:1]
TGF- β [1] Induced α-SMA, miR-195, and Smad7 Transcription in HSCs. [score:1]
Using Lipofectamine 2000 (Invitrogen), HEK 293T cells were transfected with a mixture of the pMIR-Smad7 vector and either a miR-195 mimic (50 nM) or the same concentration of scrambled miRNA (miRNA mimic negative control) as a negative control. [score:1]
MicroRNA-195 has been shown to regulate the activation of HSCs. [score:1]
In primary peritoneal carcinoma and tongue squamous cell carcinoma, miR-195 was decreased. [score:1]
The miR-195 mimics activated HSCs, further elevated miR-195 and α-SMA (P < 0.01), and reduced the Smad7 level (P < 0.05). [score:1]
The results indicated that TGF- β [1] could stimulate HSCs activation and proliferation and promote miR-195 transcription. [score:1]
Enhanced miR-195 and decreased Smad7 were observed in diethylnitrosamine -induced liver fibrotic rats (P < 0.05). [score:1]
In adrenocortical carcinoma, breast cancer, and chronic lymphoblastic leukemia, however, miR-195 was increased [16, 17]. [score:1]
In this report, we confirmed that miR-195 was increased in TGF- β [1] -induced HSCs as well as in diethylnitrosamine- (DEN-) induced rat liver fibrotic tissues. [score:1]
These data clearly indicated that elevated levels of miR-195 played a vital role in TGF- β [1]-activated HSCs. [score:1]
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2
[+] score: 144
Interestingly, masking the action of DR6 using the DR6 antibody and N-APP antibody blocked the action of downregulated miR-195 in inducing neuron death and increasing cleaved caspase-6 and caspase-3. Taken together, the results of the present study demonstrate that downregulation of miR-195 was involved in CBH -induced dendritic remo deling and neuron death by upregulation of APP and BACE1 -mediated overproduction of N-APP as well as direct upregulation of DR6 expression simultaneously. [score:16]
analysis showed that overexpression of miR-195 significantly inhibited DR6 protein level, while co-transfection of AMO-195 significantly inhibited its effect on DR6 expression (Figure 6c). [score:9]
These results indicated that miR-195 knockdown -induced dendrite degeneration and neuron loss were not only due to its action on overproduction of N-APP but also correlated with its direct action on the upregulation of DR6 expression. [score:8]
Beyond our prediction, upregulation of miR-195 by lenti-pre- miR-195 injection directly to the CA1 region of hippocampi of 2VO rats reversed the elevation of not only N-APP but also DR6 expression. [score:7]
Our previous study demonstrated that CBH -induced A β deposition in rat hippocampi and temporal lobe cortices was due to upregulation of the APP and BACE1 proteins, and these changes were regulated by the reduction of miR-195 expression. [score:7]
The next issue is that knockdown of miR-195 induced the elevation of N-APP because of its upregulating action on APP and BACE1; [23] how, then, does miR-195 affect the expression of DR6? [score:7]
4, 10, 11, 27 Our previous study reported that CBH from 2VO surgery could induce A β aggregation by upregulating both APP and BACE1 via low expression of miR-195. [score:6]
Consistent with our previous study, 23, 24 the application of lenti-pre-AMO- miR-195 inhibited miR-195 expression in rat hippocampi and cortices at the 8th week compared with that in rats injected with negative control (NC), while co-injection of lenti-pre- miR-195 reversed the reduction of miR-195 expression (Figure 3a). [score:6]
This process was regulated by the downregulated miR-195 mediated over-produced N-APP from the cleavage of APP by BACE1 following CBH, 20, 23 and regulated DR6, which is a necessary and sufficient ligand for N-APP. [score:6]
Using three strategies, we found that the tnfrsf21 gene, which encodes DR6, is the target of miR-195 and that miR-195 post-transcriptionally regulates the expression of DR6 by binding with the 3′UTR of DR6 at a position of 1563–1585 bp. [score:6]
To further clarify the direct effect of miR-195 on DR6 expression, a miRNA-masking antisense oligodeoxynucleotides (ODN) for the tnfrsf21 gene was designed and synthesized. [score:4]
As predicted, lenti-pre-AMO- miR-195 injection successfully elicited the upregulation of N-APP and DR6, which was prevented by co-injection of lenti-pre- miR-195 (Figures 3b and c). [score:4]
Accordingly, by immunofluorescence staining, the increases of cleaved caspase-6 and caspase-3 in both the hippocampi and the cortices of 2VO rats were also markedly inhibited by lenti-pre- miR-195 application (Figures 7d and e). [score:3]
We found that miR-195 mimics significantly inhibited, while AMO-195 markedly increased, the levels of cleaved caspase-6 and caspase-3, and these changes did not occur upon co-transfection of miR-195 mimics and AMO-195 (Figures 5a and b). [score:3]
Co-transfection of DR6-ODN with miR-195 into NRNs blocked the inhibitory effects of miR-195 on DR6 (Figure 6e), as was further indicated by the prevention of DR6 immunofluorescence signal reduction induced by miR-195 transfection (Figure 6f). [score:3]
[23] HEK293T cells were transfected with miR-195, AMO-195 or NC siRNAs as well as psi-CHECK-2-target DNA (firefly luciferase vector) and a blank plasmid using Lipofectamine 2000 transfection reagent (Invitrogen, USA). [score:3]
The full length of the 3′UTR of tnfrsf21 containing the miR-195 binding sites was then cloned into a luciferase -expressing reporter plasmid, and we assessed the effects of miR-195 on reporter activities in HEK293T cells. [score:3]
As predicted, the increases in N-APP and DR6 expression in both the hippocampi and the cortices of 2VO rats were prevented by lenti-pre- miR-195 injection (Figures 7b and c). [score:3]
To further demonstrate the hypothesis that knockdown of miR-195 induced dendrite degeneration and neuron loss in a manner dependent on the N-APP/DR6/caspase pathway, we used an in vitro strategy. [score:2]
Thereafter, both TUNEL and techniques were performed to observe whether knockdown of miR-195 could induce neuron death. [score:2]
Knockdown of miR-195 elicits dendrite degeneration and neuron loss both in vivo and in vitroWe next decided to explore the molecular mechanism. [score:2]
These results soundly demonstrated that knockdown of miR-195 could induce dendrite degeneration and neuron loss via the activation of the N-APP/DR6/caspase pathway. [score:2]
[34] Interestingly, gain of function of miR-195 by injection of lenti-pre- miR-195 directly into the hippocampal CA1 region of 2VO rats significantly reversed the dendritic ramification impairment of pyramidal neurons in the hippocampal CA1 and cortex as well as granular neurons in the cortex; however, it failed to prevent injury to the granular neurons in the DG region of the hippocampus. [score:2]
Knockdown of miR-195 elicits dendrite degeneration and neuron loss both in vivo and in vitro. [score:2]
As illustrated in Figure 6b, co-transfection of miR-195 with the plasmid consistently decreased the luciferase activity relative to that for transfection of the plasmid alone, whereas application of AMO-195 or mutation of the binding sites abolished the silencing effect of miR-195 (Figure 6b; for wild type: F [(4, 14)]=258.3, P<0.0001; for mutant: F [(4, 14)]=1.447, P=0.2887). [score:2]
As in our previous study, the miR-195 level was significantly increased in the hippocampi and cortices of 2VO rats when lenti-pre- miR-195 was injected (Figure 7a), suggesting the successful gain of function of miR-195 in 2VO rats. [score:1]
23, 37 The synthesis and lentivirus packaging of three single-stranded DNA oligonucleotides including pre- miR195, pre-AMO- miR-195 and NC were performed by GeneCopoeia Inc. [score:1]
The ODN was fully complementary to the predicted miR-195 binding sites in the 3′UTRs of the tnfrsf21 gene and was labeled as DR6-ODN. [score:1]
Importantly, lenti-pre-AMO- miR-195 injection also significantly reduced the dendritic length and numbers as well as the dendritic crossings of pyramidal (Figures 4e–h; for h: F [(2, 87)]=82.32, P<0.0001) and granular neurons (Supplementary Figures S1e–h) in the cortex relative to NC treated rats. [score:1]
[5] In light of our previous studies of miR-195 -mediated A β aggregation, [23] tau hyperphosphorylation through the activation of Cdk5/p25 (ref. [score:1]
We found that knockdown of miR-195 by lenti-pre-AMO- miR-195 injection elicited significantly increased positive TUNEL signals in the hippocampal CA1 area and cortex (Figure 4i) and caused decreased signals compared with sham control rats (Figure 4j); both effects were prevented by co-injection with lenti-pre- miR-195 (Figures 4i and j). [score:1]
The transfection efficiency of miR-195 and AMO-195 into NRNs was verified using qRT-PCR (Supplementary Figure S2). [score:1]
By searching the microRNA database RNAhybrid, we found that there was a miR-195 binding site within the tnfrsf21 gene, which encodes the DR6 protein, at 1563–1585 bp in the 3′UTR (Figure 6a). [score:1]
To clarify this issue, lentiviral vectors (2.0  μl) containing anti- miR-195 oligonucleotide fragments (lenti-pre-AMO- miR-195) and miR-195 oligonucleotide fragments (lenti-pre- miR-195) were developed and stereotaxically injected into the bilateral hippocampal CA1 subfields of normal rats to assess the role of miR-195 in dendrite degeneration and neuronal death. [score:1]
Co-injection of lenti-pre- miR-195 successfully prevented all the changes induced by lenti-pre-AMO- miR-195 injection (Figures 4a–h). [score:1]
We first transfected miR-195 and AMO-195 into primary cultured neonatal rat neurons (NRNs) using X-treme GENE siRNA transfection reagent. [score:1]
Gain of miR-195 reverses the dendrite degeneration and neuron loss in hippocampal CA1 and cortex induced by 2VO. [score:1]
[23] Hence, we speculated that miR-195 may affect the remo deling of dendrites. [score:1]
[23] We speculated that miR-195 might also be involved in the process. [score:1]
miR-195 mimics, AMO- miR-195 and NC were synthesized by GenePharma Corporation (Suzhou, China). [score:1]
After the skull was exposed, the bilateral hippocampi were located and 2  μl lenti-pre- miR-195 and/or lenti-pre-AMO- miR-195 was injected into CA1 of the hippocampus using a 5  μl Hamilton syringe with a 33-gauge tip needle (Hamilton, Bonaduz, Switzerland) at a rate of 30 nl/min following the drilling of a small injection hole. [score:1]
The next issue was whether miR-195 indeed plays a significant role in 2VO -induced dendrite degeneration and neuron loss. [score:1]
Gain of miR-195 reverses the dendrite degeneration and neuron loss in hippocampal CA1 and cortex induced by 2VOThe next issue was whether miR-195 indeed plays a significant role in 2VO -induced dendrite degeneration and neuron loss. [score:1]
We observed that the addition of lenti-pre-AMO -195 induced the impairment of dendritic ramification of pyramidal neurons in the hippocampal CA1 and cortex as well as granular neurons in the cortex, and these impairments were effectively prevented by co-injection of lenti-pre- miR-195. [score:1]
However, lenti-pre- miR-195 could effectively block the reduction of dendritic length and numbers of pyramidal and granular neurons in the cortex (Figures 8e–g and Supplementary Figures S3e–g) as well as dendritic crossings in both pyramidal (Figure 8h, F [(2, 81)]=9.15, P<0.001) and granular neurons (Supplementary Figure S3h) of cortical areas relative to 2VO -treated rats. [score:1]
We then evaluated whether miR-195 could affect DR6 protein expression. [score:1]
In addition, similar effects of miR-195 were observed in the changes in cleaved caspase-6 (Figure 3d) and caspase-3 (Figure 3e) by immunofluorescence staining. [score:1]
Notably, as assessed by either TUNEL staining or, lenti-pre- miR-195 did not influence the neuron death and activity in the hippocampal DG area of 2VO rats (Figures 8i and j). [score:1]
24) and inactivation of protein phosphatase-2A (PP2A), [25] our findings here demonstrated that miR-195 is a key link among the hallmarks of AD and VaD, including A β peptide aggregation, tau hyperphosphorylation, synaptic plasticity and neuron death following CBH. [score:1]
To clarify this issue, we injected the antisense of miR-195 (lenti-pre-AMO -195) into the CA1 region to mimic the injury of 2VO surgery. [score:1]
To address this query, lenti-pre- miR-195 was injected into the hippocampal CA1 region of 2VO rats. [score:1]
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3
[+] score: 128
372 inhibition -dependent reduction in ACC and FAS expression and impaired intracellular triglyceride contents could be largely restored by miR-195 suppression (Fig.   5c, Supplementary Fig.   6b, Supplementary Fig.   7a, b), suggesting that reduced miR-195 suppression of ACC and FAS expression plays a key role in uc. [score:11]
372 specifically suppresses miR-195/miR-4668 expression by binding to pri-miR-195/pri-miR-4668 to relieve miR-195/miR-4668 -mediated suppression of functional target genes such as ACC, FAS, SCD1, and CD36, leading to lipid accumulation in hepatocytes. [score:9]
372 drives hepatic steatosis through inhibition of miR-195/miR-4668 maturation to relieve miR-195/miR-4668 -mediated suppression of functional target gene related to lipid synthesis, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1), and genes related to lipid uptake such as CD36, leading to hepatic lipid accumulation. [score:7]
372 inhibits the maturation of miR-195/miR-4668 to regulate expression of ACC, FAS, SCD1, and CD36. [score:6]
b Expression levels of ACC and FAS in the HepG2 cells transfected with miR-195 mimic and inhibitor for 24 h in the presence with Ad-uc. [score:5]
372 was overexpressed, no changes in pri-miR-195/pri-miR-4668, pre-miR-195/pre-miR-4668, and mature miR-195/miR-4668 expression were identified (Supplementary Fig.   5b). [score:5]
a Expression levels of ACC and FAS in the HepG2 cells transfected with miR-195 mimic and inhibitor at a final concentration of 20 nM for 48 h (n = 3). [score:5]
372 drives hepatic steatosis by repressing the maturation of miR-195/miR-4668, thus relieving the suppression of target genes, including ACC, FAS, SCD1, and CD36. [score:5]
Additionally, miR-195 suppresses cell proliferation, invasion, and metastasis in breast cancer cells by targeting FAS, HMGCR, ACC, and CYP27B1 [26]. [score:5]
Based on the previous studies and our observations, we consider that FAS and ACC/SCD1 and CD36 are direct targets of miR-195/miR-4668 mediated by Ago2. [score:4]
Singh R Yadav V Kumar S Saini N Microrna-195 inhibits proliferation, invasion and metastasis in breast cancer cells by targeting fasn, hmgcr, acaca and cyp27b1Sci. [score:4]
Intriguingly, we observed an increase of pri-miR-195/pri-miR-4668 and a reduction of miR-195/miR-4668 expression in the liver of NAFLD patients (Fig.   8f, g). [score:3]
372 affected lipid metabolism through miR-195/miR-4668 -mediated target genes. [score:3]
Previous studies have shown that ACC and FAS are target genes of miR-195 [26] (Supplementary Fig.   6a). [score:3]
372 inhibits the maturation of miR-195/miR-4668. [score:3]
Abnormal expression of miR-195 has been wi dely reported in diverse biological systems 51, 52. [score:3]
For instance, miR-195 can bind the 3′UTRs of cyclin D1, CDK6, and E2F3, thereby suppressing cell proliferation in human hepatocellular carcinoma cells [52]. [score:3]
372, we determined expression levels of pri-miR-195/pri-miR-4668, pre-miR-195/pre-miR-4668, and miR-195/miR-4668 upon uc. [score:3]
372i-infected and miR-195 inhibitor -transfected HepG2 cells in the presence with with 300 μM O/P mixture for 48 h (representative blots from three similar experiments) (n = 3). [score:3]
As shown by real-time PCR analysis, miR-195 markedly suppressed mRNA levels of FAS and ACC, even when uc. [score:3]
Consistently, we found that miR-195 markedly suppresses mRNA levels of FAS and ACC, even when uc. [score:3]
In the present study, the sequence alignment results in Supplementary Fig.   6a, b showed canonical complementarity between miR-195/miR-4668 and their respective targets, which is necessary for the formation of the miRNA–mRNA duplex [56]. [score:3]
372 on abnormal lipid accumulation is subjected to regulation of miR-195/ miR-4668 in the liver of NAFLD patients. [score:2]
372 was functionally involved in the abnormal hepatic lipid accumulation of NAFLD patients by regulation of pri-miR-195/pri-miR-4668 processing. [score:2]
Liu L Chen L Xu Y Li R Du X Microrna-195 promotes apoptosis and suppresses tumorigenicity of human colorectal cancer cellsBiochem. [score:2]
372 regulates pri-to-pre-miRNA cleavage of miR-195 and 4668 by binding pri-miR-195/pri-miR-4668. [score:2]
372 is subject to regulation by miR-195/miR-4668 in the steatotic liver of NAFLD patients. [score:2]
372 binds to pri-miR-195/pri-miR-4668. [score:1]
372 and the terminal loop region of pri-miR-195/pri-miR-4668. [score:1]
How miR-195/miR-4668 link to the metabolic genes such as FAS, ACC, SCD1, and CD36? [score:1]
f The levels of pri-miR-195, pre-miR-195, and mature miR-195 in the liver samples of NAFLD patients or healthy control (n = 11). [score:1]
283 + A impairs microprocessor recognition and efficient pri-miR-195 cropping [22]. [score:1]
TRIzol reagent (Invitrogen) was used to isolate the precipitated RNA and the level of pri-miR-195 or pri-miR-4668 was further analyzed using real-time PCR. [score:1]
372. e The levels of pri-miR-195/pri-miR-4668, pre-miR-195/pre-miR-4668, and mature miR-195/miR-4668 in the HepG2 cells transfected with Ad-uc. [score:1]
Subsequently, we analyzed the hepatic levels of pri-miR-195/pri-miR-4668 and mature miR-195/miR-4668 in these patients. [score:1]
372 significantly increased the level of pri-miR-195/pri-miR-4668 in the immunoprecipitated RNA with antibody against Drosha, indicating a binding between uc. [score:1]
Of note, pri-miR-195 and pri-miR-4668 displayed a complementarity with the ultraconserved region of uc. [score:1]
To further assess that pri-miR-195/pri-miR-4668 interacts with uc. [score:1]
This complementarity involved nucleotides located at the terminal loop region site within the miR-195 and miR-4668 primary transcripts (Fig.   4d). [score:1]
To explore the interaction between miR-195/miR-4668 and uc. [score:1]
372 could bind pri-miR-195/pri-miR-4668 in HepG2 cells transfected with Ad-uc. [score:1]
372 at the terminal loop region site within the miR-195 and miR-4668 primary transcript. [score:1]
Based on the reduced levels of miR-195 in HepG2 cells treated with an O/P mixture (Supplementary Fig.   6a), we investigated the effects of miR-195 on expression of ACC and FAS. [score:1]
d The stem-loop sequence of pri-miR-195 (left panel) and pri-miR-4668 (right panel), and their partial complementarity with uc. [score:1]
372 in the HepG2 increased the levels of pri-miR-195/pri-miR-4668 and repressed the maturation of miR-195/miR-4668 (Fig.   4e). [score:1]
Of note, significantly reduced pri-miR-195/pri-miR-4668 and elevated pre-miR-195/pre-miR-4668 and mature miR-195/miR-4668 were observed in the HepG2 cells transfected with Ad-372i (Supplementary Fig.   5a). [score:1]
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4
[+] score: 30
Specifically, miR-195 potentially regulates vesicle -associated membrane protein 1 (VAMP1), miR-30a targets actinin, alpha 1 (ACTN1), miR-21 targets paired-like homeodomain 2 (PITX2) in D6; miR-132 potentially regulates solute carrier family 2, member 1 (SLC2A1), nuclear receptor subfamily 4, group A, member 2 (NR4A2) and Cdc42 guanine nucleotide exchange factor 9 (ARHGEF9), miR-203 targets calcium binding protein 7 (CABP7), miR-17-5p targets early growth response 2 (EGR2) in S6; miR-330 potentially regulates CD247, nerve growth factor receptor (NGFR) and FAT tumor suppressor homolog 3 (FAT3), miR-338 targets ADAM metallopeptidase domain 17 (ADAM17), miR-218 targets src kinase associated phosphoprotein 1 (SKAP1), miR-185 targets calcium channel, voltage -dependent, N type, alpha 1B subunit (CACNA1B) in S9. [score:20]
Specially, miR-195 and miR-30a could contribute to the regulation of BDNF expression in human prefrontal cortex [32]. [score:4]
It is, therefore, intriguing to speculate that miRNAs, including miR-195, miR-30a and miR-21 (in D6), may participate in a molecular network involving multiple reciprocal nodes that together orchestrate and fine-tune diverse targets and signaling in axon outgrowth. [score:3]
VAMP1, the target of miR-195, was involved in synaptic vesicle recycling and exocytosis in neurons [33]. [score:3]
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5
[+] score: 26
We identified 2 miRNAs (miR-195 and miR-200c) that were distinctively expressed in the rat lung, 8 miRNAs that were co-expressed in the lung and heart and 1 miRNA that was co-expressed in the lung and kidney. [score:7]
Statistical analysis using Significant Analysis of Microarray (SAM) and Tukey Honestly Significant Difference (HSD) revealed 2 miRNAs (miR-195 and miR-200c) expressed specifically in the lung and 9 miRNAs co-expressed in the lung and another organ. [score:5]
Also, miR-195 was previously reported to be expressed higher in the spleen than in the lung [37], but both our microarray and Northern blot results show rno-miR-195 expressing much higher in the lung than in the spleen. [score:5]
Two miRNAs (rno-miR-195 and rno-miR-200c) were identified as being expressed specifically in the rat lung. [score:3]
In a few cases, the Northern blot showed a higher expression in comparison with the microarray, including miRNA-195 in heart and miRNA-145 in kidney and spleen. [score:3]
Among the 12 selected miRNAs, two were lung-specific (miR-195 and miR-200c), one was kidney-specific (miR-10a), and three were co-expressed in the lung and heart (miR-126, miR-143 and miR-145) as determined by HSD, OSI and two-fold criteria. [score:3]
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6
[+] score: 26
mir-200a, mir-34, mir-195, and mir-381-3p are usually downregulated in presence of SIRT1 expression, and vice versa low expression of SIRT1 relates to miRNAs upregulation [9, 11, 17, 18, 26– 28]. [score:11]
Comparing the miRNAs expression of LPS -treated rats with LPS + RvD1, a significant downregulation of the levels of miR-195-5p, miR-200a-3p (related to SIRT1 expression and activity), miR-145-5p (related to both SIRT1 and p53 regulation), and miR-34a-5p (candidate for p53 regulation) in ocular tissues of LPS + RvD1 1000 ng/kg treated rats compared to the LPS -treated group (P < 0.01 versus LPS group; Figure 6) was noted. [score:9]
Interestingly, the protective action of intravitreal RvD1 was associated with an increased level of endogenous SIRT1 within the eye and a downregulated expression of miR-195-5p, miR-200a-3p, miR-34a-5p, and miR-145-5p. [score:6]
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7
[+] score: 26
Amongst these, miR-383 was differentially expressed in all three rats and up-regulated to the largest degree in rat one, and the ten other miRNAs, let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592 and miR-1224 were differentially expressed in at least two rats. [score:8]
In these 10 deregulated miRNAs, seven (let-7d*, miR-181b, miR-187, miR-214, miR-466b, miR-592, miR-1224) are up-regulated in two rats, and one (miR-195) is down-regulated. [score:8]
In dysregulated miRNAs, let-7d*, miR-181b, miR-187, miR-214, miR-383, miR-466b, miR-592, miR-1224 are significantly overexpressed in MrD compared to hippocampus, and miR-195 is downexpressed. [score:5]
Hence, miR-383 was differentially expressed in three rats, and let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592, miR-1224 were differentially expressed in two rats at least (Additional file 2: Table S4). [score:5]
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8
[+] score: 16
b The short peptide, ERAP, and the natural product derived from medical plants, xanthohumol, could disrupt the PHB2/BIG3 interaction directly and lead to the translocation of PHB2 from cytoplasm to nucleus, thereby, induce cell growth arrest in some estrogen -dependent cancers a PHB1 can be down-regulated by miR-26a, miR-27a, and miR-195; the lncRNA named PHBP1 directly binds to and maintain the stabilization of PHB1 mRNA; the acetylation of histone H3 can also increase the expression of PHB1; phosphorylation of PHB1 at different amino acids determines the activation and function of PHB1. [score:8]
Fig. 4 a PHB1 can be down-regulated by miR-26a, miR-27a, and miR-195; the lncRNA named PHBP1 directly binds to and maintain the stabilization of PHB1 mRNA; the acetylation of histone H3 can also increase the expression of PHB1; phosphorylation of PHB1 at different amino acids determines the activation and function of PHB1. [score:7]
In human melanoma cells, studies showed that miR-195 binds to the 3′-UTR of PHB1 as well [119]. [score:1]
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9
[+] score: 14
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
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10
[+] score: 12
Similarly, miR-195 (predicted to target BDNF), and let-7b and miR-98 (both predicted to target NGF) have been shown previously in human muscle to increase with aging [45], consistent with our analysis in VO rat muscle. [score:5]
org) revealed several target sites for BDNF: miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p, and miR-497-5p that were conserved in humans. [score:3]
In VO rat muscle, miR-206-3p, miR-195-5p, and miR-497-5p were increased significantly. [score:1]
MicroRNAs predicted to influence neurotrophins: a BDNF (miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p and miR-497-5p), b NT3 (miR-21-5p, miR-222-3p and miR-221-3p), and c NGF (let-7b-5p and miR-98-5p) were quantified by qPCR analysis in YA (n = 8) vs VO (n = 10) rat vastus lateralis muscle and WT (n = 8) vs Sarco (n = 7) gastrocnemius muscle. [score:1]
In contrast to the aforementioned studies in aging muscle, most of the miRNAs studied herein have been examined in the context of experimental denervation, including miR-206 (increases after reinnervation), miR-10a-5p (increases four- to seven-fold with denervation), miR-1 (increases up to 10-fold following denervation and remains elevated after reinnervation), miR-195 (increases up to 10-fold with denervation), miR-21 (increases with denervation), miR-221 (no consistent change), miR-222 (no consistent change), and miR-98 (increases up to 10-fold with denervation) [43, 47, 48]. [score:1]
For BDNF, our analysis identified increases in miR-206-3p, miR-195-5p, and miR-497-5p in VO rat muscle. [score:1]
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11
[+] score: 11
However, miR-15b, miR-16, miR-20a, miR-20b [17], [18], miR-205 [23] and miR-195 [22] down-regulate angiogenesis by directly targeting VEGF. [score:7]
Recent studies also indicate that a panel of miRNAs (i. e., miR-10, miR-15b, miR-16, miR-20a, miR-20b, miR-27a, miR-126, miR-145, miR-195, miR-205, and miR-210) is involved in the regulation of VEGF expression in ECs and tumor cells [16]– [26]. [score:4]
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12
[+] score: 11
The Effect of 2 Weeks of CMS on the Expression Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p in Mesocortical Pathway. [score:3]
miR-195-5p regulates serotonergic signaling and BDNF level—two biochemical pathways strongly involved in pathophysiology of mental illness [29]. [score:2]
Moreover, statistical analysis showed that stress exposure for two consecutive weeks also decreased the expression levels of all examined miRNAs (except miR-34a-5p, see Fig. 3b) in rat PCx (Fig. 3a, c–f) as compared to control group of rats (miR-18a-5p F [2,29] = 14.19, p < 0.0001; miR-135a-5p F [2,29] = 16.95, p < 0.0001; miR-195-5p F [2,29] = 4.13, p < 0.02; miR-320-3p F [2,29] = 10.57, p < 0.001; miR-674-3p F [2,29] = 4.03, p < 0.05; miR-872-5p F [2,29] = 15.67, p < 0001). [score:2]
One-way ANOVA revealed increased expression levels of all miRNAs of interest (except miR-135a-5p, see Fig. 3c) after 2 weeks of CMS in VTA (Fig. 4a, b, d–g) of stressed animals as compared to non-stressed group of rats (miR-18a-5p F [2,29] = 4.34, p < 0.05; miR-34a-5p F [2,29] = 8.03, p < 0.01; miR-195-5p F [2,29] = 12.88, p < 0.001; miR-320-3p F [2,29] = 11.31, p < 0.001; miR-674-3p F [2,29] = 19.99, p < 0.0001; miR-872-5p F [2,29] = 18.18, p < 0.0001). [score:2]
Dynamic Changes in the Serum Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p during 2 Weeks of the CMS Procedure. [score:1]
Based on our previous study [20] and literature survey, we chose a set of seven different miRNAs (i. e., miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, miR-872-5p) which are associated with stress response and functioning of the central nervous system. [score:1]
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13
[+] score: 11
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]
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]
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14
[+] score: 11
These results indicated the expression of rno-miR-344b-3p, rno-miR-195-3p, rno-miR-30b-3p, and rno-miR-34a-5p was significantly upregulated in rats with adriamycin -induced nephropathy, whereas triptolide treatment could reverse the elevated expression of rno-miR-344b-3p and rno-miR-30b-3p to normal levels. [score:8]
Chip analysis showed that, compared to that observed in the normal group, 19 miRNAs were significantly upregulated (rno-miR-344b-3p, rno-miR-195-3p, rno-miR-30b-3p, rno-miR-34a-5p, etc. ) [score:3]
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[+] score: 10
Bish et al. [14] reported that strong cardiac shPLB expression in canines altered the expression of several miRs and induced toxic side effects such as transiently increased serum levels of troponin I. To investigate whether scAAV6-shPLBr and scAAV6-amiR155-PLBr treatment might affect the expression levels of selected cardiac miRs that had been analyzed in the in vivo study of Bish et al. [14], the levels of miR-1, miR-21, miR-124, miR-195 and miR-199a were determined in CM at day 14 after transduction with 25×10 [3] vg/c of scAAV6-shPLBr, scAAV6-amiR155-PLBr, scAAV6-shCon or scAAV6-amiR155-Con. [score:5]
To analyse the expression of miR-1, miR-21, miR-124, miR-195, and miR-199a, 10 ng of total RNA, isolated from CM, were reverse transcribed using the TaqMan MicroRNA Reverse Transcription Kit (Life Technologies, Applied Biosystems Inc. [score:3]
Expression levels were determined by real-time PCR using the TaqMan MicroRNA Assays rno-miR1, hsa-miR21, hsa-miR124, hsa-miR195 and hsa-miR199a (Life Technologies, Applied Biosystems Inc. [score:2]
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[+] score: 9
So we paid more attention to miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497, which are the targeted results for CX3CL1 in the Targetscan Database. [score:5]
In order to investigate whether some micro -RNA contained in the MVs played a role, we searched CX3CL1 in the TargetScan database (version 6.2) and identified six putative micro -RNA (miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497) targets to CX3CL1 mRNA by matching the seed regions of each. [score:3]
The real-time quantitative PCR analysis indicated that there were relatively high levels of miR-15a, miR-15b and miR-16 contained in hWJMSC-MVs, but none or low levels of miR-195, miR-424 and miR-497 (Figure  7B). [score:1]
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[+] score: 9
In response to 4 hours of mechanical stretch, rno-miR-322, let-7f, miR-103, miR-126, miR-494, miR-126*, miR-130b and miR-195 were significantly dysregulated (Fig.   7A and Supplementary Dataset  5), so we sought potential mRNA targets for these dysregulated miRNAs among the stretch-regulated genes in 4 and 12 hours timepoints. [score:6]
In response to 1 hour of mechanical stretching, only one miRNA, rno-miR-130b showed differential expression compared to controls (P < 0.05), whereas 8 miRNAs (rno-miR-322, rno-let-7f, rno-miR-103, rno-miR-126, rno-miR-494, rno-miR-126*, rno-miR-130b, rno-miR-195; P < 0.05) were dysregulated in response to 4 hours of stretch (Supplemental Dataset  5). [score:3]
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[+] score: 9
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
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[+] score: 8
Our previous work also revealed that the heart failure of the rat with selenium deficiency was probably related to five upregulated miRNAs (miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e) and three downregulated miRNAs (miR-3571, miR-675 and miR-450a) [11]. [score:7]
Of these miRNAs, such as rno-miR-16, rno-miR-199a-5p, rno-miR-195, rno-miR-30e, which had been reported to be involved in selenium deficiency induced heart failure [11]. [score:1]
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[+] score: 8
Nine miRNAs (miR-21, miR-24, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) were found in exosomes obtained from rats subjected to RIPC, but only miR-24 was significantly upregulated ([#] P < 0.05, n = 4). [score:4]
b, c Flow cytometric analysis of the uptake of exosomes by H9c2 cells at various time points We further determined the expression of nine miRNAs (miR-24, miR-21, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) in both RIPC-EXO and EXO (Fig.   3a). [score:3]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
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21
[+] score: 7
Similarly, the specific miRNA profile of AFL consisted of five downregulated (miR-93, miR-451, miR-221, miR-17-5p and miR-146a) and three upregulated (miR-200c, miR-490 and miR-195) miRNAs, in comparison to the control group. [score:7]
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[+] score: 6
In addition, Itesako et al. concluded that down-regulation of miR-195/497 cluster contributed to bladder cancer progression by targeting BIRC5 and WNT7A genes [24]. [score:6]
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23
[+] score: 6
For example, in the spinal nerve ligation mo del, intrathetal injections of miR-21 (Sakai and Suzuki, 2013), miR-103 (Favereaux et al., 2011), miR-183 (Lin et al., 2014) or of miR-195 inhibitor (Shi et al., 2013), and injection of miR-7a into the L5-DRG (Sakai et al., 2013) attenuate pain. [score:3]
Increased miR-195 aggravates neuropathic pain by inhibiting autophagy following peripheral nerve injury. [score:3]
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24
[+] score: 6
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-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, Landgraf et al. [18] studied the mammalian miRNA expression atlas by sequencing 250 small RNA libraries representing 26 different human and rodent organ systems and cell types, and Wang et al. [21] used home-made miRNA microarrays to identify the rat lung-specific miRNAs, miR-195 and miR-200c. [score:3]
Wang et al. [21] investigated the tissue-specific expression of miRNAs in six rat tissues (lung, heart, brain, kidney, liver and spleen), and found that miR-195 and miR-200c were expressed specifically in the lung. [score:3]
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25
[+] score: 6
Our findings were similar to the study by Hang et al. which showed that BDNF by downregulating microRNA-195 inhibited cardiac apoptosis and attenuated myocardial ischemia reperfusion injury in rats [38]. [score:6]
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[+] score: 6
Our data provide evidence for the downregulation of the microRNAs miR195 and miR30a, which have been shown to target the growth factor BDNF [105]. [score:6]
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[+] score: 5
Hang P Sun C Guo J Zhao J Du Z BDNF-mediates Down-regulation of MicroRNA-195 Inhibits Ischemic Cardiac Apoptosis in RatsInt J Biol Sci. [score:5]
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The miR-15 family members including miR-15a, miR-15b, miR-16, miR-195, miR-424, and miR-497, show 5′-end sequence similarity and many common targets [16, 17]. [score:3]
It has been demonstrated that miR-195 is pro-apoptotic in cardiomyocytes [20]. [score:1]
It was reported miR-195 increases cardiac hypertrophy [27] and worsens systolic dysfunction in mice with MI [17], while miR-15b, another member of the same miR-15 family, was found to attenuate myocardial fibrosis and hypertrophy in pressure-overloaded mice [19]. [score:1]
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29
[+] score: 4
Other miRNAs from this paper: rno-mir-30a
Activation of Cdk5/p25 and tau phosphorylation following chronic brain hypoperfusion in rats involves microRNA-195 down-regulation. [score:4]
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30
[+] score: 4
Other miRNAs from this paper: hsa-mir-195
Endothelin-1–Induced Macrophage Inflammatory Protein-1β Expression in Monocytic Cells Involves Hypoxia-Inducible Factor-1α and AP-1 and Is Negatively Regulated by microRNA-195. [score:4]
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31
[+] score: 4
Interestingly, among the miRNAs found to be upregulated in exosomes in response to cytokines, several of them including miR-146a, miR-146b, miR-195, miR-290a-3p, miR-362-3p and miR-497 are known to be involved in cell death [29- 34]. [score:4]
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32
[+] score: 3
GRN expression is also under the post-transcriptional control of miR-107 (a member of a miRNA group also including miR-15, miR-16, miR-103, miR-195, miR-424, miR-497, miR-503, and miR-646), with implications for brain disorders (Wang et al., 2010). [score:3]
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33
[+] score: 3
For example, it has been reported that miR-221 [15], miR-199a/b [16][17], miR-27b [18], miR-195 [11] and miR-34a/b/c [19] positively regulate cardiac hypertrophy, while miR-378 [9], miR-29 [20], miR-150 [11], miR-223 [21] and miR-1 [22] negatively regulate cardiac hypertrophy. [score:3]
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34
[+] score: 3
For example, miR-195, miR-497, and miR-30b were found to be enriched in the cerebellum whereas miR-218, miR-221, miR-222, miR-26a, miR-128a/b, miR-138 and let-7c were highly expressed in the HIP. [score:3]
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35
[+] score: 3
Furthermore, in diabetic conditions, expression levels of miR-195 and miR-29 have been shown to be elevated and reduced, respectively, in podocytes where they play a role in apoptosis and fibrosis [4]. [score:3]
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36
[+] score: 3
283A impairs the proper RNA processing machinery of pri-miR-195 and reduces the production of mature miR-195, which in turn leads to the derepression of many miR-195 targets related to cell proliferation 13. [score:3]
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37
[+] score: 3
There are several other miRNAs, such as miR-7, miR-124a, miR-9, miR-34a and miR-195, that play a role in the regulation of insulin secretion and β cell development [17]. [score:3]
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38
[+] score: 2
Several candidate therapeutic miRNAs have progressed into clinical and preclinical development; for example, antisense miR-122 is being developed as a treatment for hepatitis C virus, miR-208/499 for chronic heart failure, miR-195 for myocardial infarction and miR-34 and let-7 for cancer 10, 11. [score:2]
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39
[+] score: 2
In all, we found moderate (three-fold) region-specific enrichment of 48 miRNAs (e. g. miR-138, miR-195 and miR-218, Figure S2). [score:1]
In line with previous studies in mice, we also found moderate enrichment of miR-195 [39], [40] in the cerebellum and of miR-218 in the hippocampus [39] (Figure S2). [score:1]
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40
[+] score: 2
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]
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]
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41
[+] 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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42
[+] score: 1
with and without species identifiers (e. g. hsa-miR-195 and miR-195). [score:1]
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43
[+] score: 1
Other miRNAs from this paper: mmu-mir-195a, hsa-mir-195, mmu-mir-195b
283+A was shown to decrease pri-miR-195 biogenesis by impairing microprocessor recognition and pri-miRNA cropping [16]. [score:1]
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44
[+] score: 1
They were miR-1, miR-21, miR-195 and miR-200c. [score:1]
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45
[+] score: 1
miR-16 located at 13q14, which is identified as miR-15 miRNA cluster that includes miR-15a, miR-15b, miR-16, miR-195, and miR-497 [25]. [score:1]
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46
[+] score: 1
This ncRNA-ncRNA interaction prevents pri-miRNA-195 cleavage by Drosha. [score:1]
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47
[+] score: 1
On the other hand, miR-191a-5p and -29a-3p showed significant changes only in rats supplemented with BMFC; while miR-195-3p and -148a-5p were the only miRNAs significantly affected in the combined-supplement group. [score:1]
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48
[+] 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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49
[+] score: 1
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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