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14 publications mentioning rno-mir-185

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-185. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 278
In the same context, mutations of the target sites in the 3′-UTR completely blocked the inhibitory effects of miR-185, suggesting that the identified sites, shown in Figs. 3B-3D, are the direct target sites for miR-185 regulation. [score:10]
Treatment with a specific inhibitor for miR-185 markedly down-regulated miR-185 expression (Figure E in S1 File) and accelerated ET-1 induced cardiomyocytes hypertrophy, as shown in Figs. 1E-1H. [score:8]
To confirm these target predictions, we transfected miR-185 into NRVMs and determined whether endogenous levels of those target genes were down-regulated. [score:8]
As expected, the levels of CaMKIIδ phosphorylation at Thr-286 and total CaMKIIδ were significantly lower in miR-185 -overexpressing cardiomyocytes compared with the levels in the control group (Fig. 5A), while inhibition of miR-185 significantly up-regulated phosphorylation of CaMKIIδ at Thr-286 and the amount of total CaMKIIδ (Fig. 5B). [score:7]
Inhibition of NCX1 by 1 μM SEA0400 (2-[4-[(2,5-difluorophenyl) methoxy] phenoxy]5-ethoxyaniline), a potent NCX1 inhibitor [43], also reduced cardiomyocyte size and expression of the hypertrophic markers, ANF and BNP, to a similar extent (Figure I in S1 File), demonstrating that anti-hypertrophic effect of miR-185 is due, in part, to repression of Ncx1. [score:7]
The previous studies have also identified additional miR-185 target genes, such as RhoA, Cdc42, and Stim1 [65– 69], that are pro-hypertrophic in the heart, suggesting further that miR-185 is a strong anti-hypertrophic miRNA in vivo and a potent therapeutic target for cardiac diseases. [score:7]
As shown in Figure G in S1 File, over -expression of miR-185 significantly inhibited ISO- or PE -induced cardiomyocyte hypertrophy as assessed by cell surface area and hypertrophic marker gene expressions. [score:7]
Cells were then transfected with 15 nmol/L miRIDIAN microRNA mimic rno-miR-185, miRIDIAN microRNA mimic negative control #1 (NC), 100 nmol/L of miRIDIAN microRNA hairpin inhibitor rno-miR-185, and miRIDIAN microRNA hairpin inhibitor negative control #2 (NC inhibitor) using DharmaFECT-3 reagent (all obtained from Dharmacon) according to the manufacturer’s instructions. [score:7]
Consistent with the previous report [12], we found that the expression of miR-185 was dramatically down-regulated after TAC, reached a minimal level on day 7 (Figure D in S1 File). [score:6]
Transgenic expression of microRNA-185 causes a developmental arrest of T cells by targeting multiple genes including Mzb1. [score:6]
Finally, miR-185 has 22 high score targets in cardiac hypertrophy signaling pathway, as determined by cross-species target predictions (Figure B in S1 File). [score:5]
We propose that miR-185 is a potential drug target for diseases such as heart failure. [score:5]
Briefly, 9xNFAT-luciferase reporter plasmid and pRL-TK containing the Renilla luciferase gene were cotransfected into NRVMs 24 h after transfection of NC inhibitor or miR-185 inhibitor. [score:5]
Based on our identification of Camk2d as a target of miR-185 (Fig. 3B), we performed western blotting to examine the level of p-CaMKIIδ after transfection of miR-185 mimic or miR-185 inhibitor. [score:5]
In the present study, we demonstrated that miR-185 leads to inhibition of these Ca [2+]-activated hypertrophic pathways by simultaneously targeting Camk2d and Nfatc3 and the reduction of their activities. [score:5]
For miRNA target identification, we constructed reporter vectors bearing the exact target sites for miR-185. [score:5]
Data represent the mean ± SEM; * P < 0.05, ** P < 0.001, N = 4. Next, we determined whether Camk2d, Ncx1, and Nfatc3 are the direct targets of miR-185. [score:4]
Interestingly, miR-185 is the most representative down-regulated miRNA, implying that depletion of miR-185 substantially contributes to the cardiac defects in the syndrome [64]. [score:4]
0122509.g003 Fig 3 miR-185 directly targets 3′-UTR of Camk2d, Ncx1, and Nfatc3. [score:4]
miR-185 directly targets multiple key components in the calcium-activated hypertrophic signaling pathway. [score:4]
The results showed that both mRNA and protein expression levels of calcium/calmodulin -dependent protein kinase II delta (CaMKIIδ), Na [+]-Ca [2+] exchanger gene (NCX1/SLC8A1), and NFATC3 were significantly repressed by miR-185 compared with expression in the controls (Fig. 2A-F). [score:4]
miR-185 directly targets multiple key components in the calcium-activated hypertrophic signaling pathwayWe next screened for components in the cardiac hypertrophy signaling cascade that are controlled by miR-185. [score:4]
In contrast, overexpression of miR-185 significantly induced phosphorylation of NFATC3, while significantly decreasing the total NFATC3, as assessed by western blotting (Fig. 4C), suggesting that miR-185 negatively regulates calcineurin-NFAT signaling. [score:4]
miR-185 directly targets 3′-UTR of Camk2d, Ncx1, and Nfatc3. [score:4]
The data are expressed as mean ± SEM of more than three independent experiments; * P < 0.05, ** P < 0.001. miR-185 modulates CaMKIIδ activity in vitro Binding of Ca [2+]/calmodulin to the regulatory domain leads activates CaMKIIδ, and the activated enzyme is subsequently autophosphorylated at Thr-286/287, rendering the kinase constitutively active [27]. [score:4]
Data represent the mean ± SEM; * P < 0.05, ** P < 0.001, N = 4. Next, we determined whether Camk2d, Ncx1, and Nfatc3 are the direct targets of miR-185. [score:4]
0122509.g002 Fig 2 miR-185 regulates the expression of CaMKIIδ, NCX1, and NFATC3 in cultured NRVMs. [score:4]
miR-185 regulates the expression of CaMKIIδ, NCX1, and NFATC3 in cultured NRVMs. [score:4]
Data represent the mean ± SEM; ** P < 0.001, or NS (not significant), N = 3. miR-185 regulates NFAT activity in vitro Based on evidence concerning the regulation of calcineurin-NFAT signaling by miR-185 (Fig. 3C, Figures B and J in S1 File), we further examined whether inhibition of miR-185 could activate calcineurin -dependent NFAT transcription factor by luciferase reporter assay employing a reporter under transcriptional control of nine NFAT binding sites (Fig. 4A). [score:4]
In conclusion, the present study shows novel evidence that miR-185 acts as a key regulator of cardiac hypertrophy by targeting three major genes involved in Ca [2+] -associated pathological hypertrophy. [score:4]
To further substantiate the inhibitory role of miR-185, we performed knockdown experiments. [score:4]
The expression of miR-185, however, is not regulated by ET-1 itself (Figure F in S1 File). [score:4]
The cells then were transfected with miRNA mimic or hairpin inhibitor for miR-185, or for the negative control, with DharmaFECT-3 reagent. [score:3]
Twenty-four hours after transfection with miR-185 (15 nmol/L) (A) or miR-185 inhibitor (100 nmol/L) (E), NRVMs were stimulated with ET-1 for 48 h. Scale bar = 50 μm. [score:3]
Data represent the mean ± SEM; ** P < 0.001, or NS (not significant), N = 3. Based on evidence concerning the regulation of calcineurin-NFAT signaling by miR-185 (Fig. 3C, Figures B and J in S1 File), we further examined whether inhibition of miR-185 could activate calcineurin -dependent NFAT transcription factor by luciferase reporter assay employing a reporter under transcriptional control of nine NFAT binding sites (Fig. 4A). [score:3]
Second, miR-185 is expressed primarily in the heart, brain and kidney [26], suggesting a potential role in these tissues. [score:3]
With regard to miR-185, pathways for TGF-β, BAD and VEGF were also predicted to be closely linked to miR-185 targets (Figure J in S1 File and S2 Table), implying that miR-185 may also affect multiple signal transductions in the heart and may play additional roles in cardiac pathogenesis. [score:3]
Among 18 candidate miRNAs, we found that miR-185 plays a significant anti-hypertrophic role in the heart through multiple targets in Ca [2+]-signaling. [score:3]
Working mo del illustrating the multiple targets of miR-185 in the calcium -dependent cardiac hypertrophy signaling pathway. [score:3]
We found that miR-185 plays an important anti-hypertrophic role in the heart and it has three major targets involved in the hypertrophic processes such as Ncx1, Nfatc3, and Camk2d (Fig. 6). [score:3]
The results showed that luciferase activity at Site 2 of Camk2d, and at Site 1 of Nfatc3 and Ncx1, which are highly conserved across species, was significantly suppressed by miR-185. [score:3]
The data are expressed as mean ± SEM; * P < 0.05, ** P < 0.001, N = 3. Since Thr-17 and Ser-16 of phospholamban (PLB) are independently phosphorylated by CaMKIIδ and cAMP -dependent protein kinase (PKA), respectively [28], we assessed phosphorylation of PLB at Thr-17 as an index of endogenous CaMKIIδ activity in NRVMs after transfection of miR-185 mimic or NC mimic. [score:3]
All data are expressed as mean ± SEM; * P < 0.05, ** P < 0.001; N = 4. miR-185 was selected for further study due to the following reasons: First, miR-185 was consistently found across four different cardiac hypertrophy signaling pathways. [score:3]
0122509.g006 Fig 6Working mo del illustrating the multiple targets of miR-185 in the calcium -dependent cardiac hypertrophy signaling pathway. [score:3]
All data are expressed as mean ± SEM; * P < 0.05, ** P < 0.001; N = 4. We next screened for components in the cardiac hypertrophy signaling cascade that are controlled by miR-185. [score:3]
Data represent the mean ± SEM; ** P < 0.001, or NS (not significant), N = 3. (A-C) analyses of Camk2d, Ncx1 and Nfatc3 expression after transfection with miR-185 or NC. [score:3]
Third, miR-185 is differentially expressed in the heart of pressure overload -induced cardiac hypertrophy mo dels [12]. [score:3]
However, it remains to be seen whether the delivery of miR-185 or transgenic over -expression of miR-185 attenuates cardiac hypertrophy in vivo. [score:3]
Consistent with the change in CaMKIIδ autophosphorylation at Thr-286, overexpression of miR-185 significantly reduced phosphorylation of PLB at Thr-17 compared with control group (Fig. 5C), demonstrating that miR-185 is directly involved in the modulation of the CaMKIIδ activity. [score:3]
The data are expressed as mean ± SEM; * P < 0.05, ** P < 0.001, N = 3. Since Thr-17 and Ser-16 of phospholamban (PLB) are independently phosphorylated by CaMKIIδ and cAMP -dependent protein kinase (PKA), respectively [28], we assessed phosphorylation of PLB at Thr-17 as an index of endogenous CaMKIIδ activity in NRVMs after transfection of miR-185 mimic or NC mimic. [score:3]
However, transfection of miR-185 mimic significantly reduced the mRNA expression of ANF and BNP in NRVMs (Fig. 1C and 1D). [score:3]
Collectively, our results suggest that miR-185 have multiple targets in the Ca [2+] -dependent cardiac hypertrophy signaling pathway. [score:3]
Data represent the mean ± SEM; * P < 0.05, ** P < 0.001, N = 4. (A) Schematic diagram of the pmirGLO chimeric vector indicating where the exact complement target sequences for miR-185 or mutant sequences were cloned into the 3′-UTR of the luciferase gene. [score:3]
To critically examine the interactions between miR-185 and the putative targets, we measured the activity of the luciferase reporter when linked to either the WT or mutant 3′-UTR of each target (Fig. 3A). [score:3]
Quantitative real-time PCR (qRT-PCR) analysis of miR-185 expression was conducted on cardiac fibroblasts at passage 3. Cardiomyocytes were seeded at a density of 0.9 million cells per dish onto 1% gelatin-coated 60-mm (Corning) culture dishes and cultured overnight in DMEM supplemented with 10% FBS, 1% antibiotics (WelGENE), 0.1 mmol/L BrdU at 37°C in a humidified incubator with 5% CO [2]. [score:3]
Collectively, the results indicate that miR-185 negatively regulates cardiac hypertrophy. [score:2]
miR-185 negatively regulates cardiac hypertrophyAmong the identified 18 miRNAs through GSA, six were previously unknown. [score:2]
miR-185 negatively regulates the activity of CaMKIIδ in NRVMs. [score:2]
Transfection of NRVMs with miR-185 inhibitor led to marked induction of the NFAT -dependent luciferase activity compared with the controls for the basal state and for the ET-1 stimulation (Fig. 4B). [score:2]
miR-185 regulates NFAT activity in vitro. [score:2]
The result suggests that miR-185 may be a critical, quick-responder, regulating cardiac hypertrophy in response to increased biomechanical stress. [score:2]
0122509.g004 Fig 4 miR-185 negatively regulates NFAT activity in NRVMs. [score:2]
qRT-PCR for miR-185 targets and hypertrophic markers was performed with primers listed in Table B in S1 File, using SYBR green dye (Kapa Biosystem) and StepOne Plus Real Time PCR System (Applied Biosystems). [score:2]
0122509.g001 Fig 1 miR-185 negatively regulate cardiomyocyte hypertrophy. [score:2]
miR-185 negatively regulates NFAT activity in NRVMs. [score:2]
for miR-185 targets and hypertrophic markers was performed with primers listed in Table B in S1 File, using SYBR green dye (Kapa Biosystem) and StepOne Plus Real Time PCR System (Applied Biosystems). [score:2]
miR-185 negatively regulate cardiomyocyte hypertrophy. [score:2]
miR-185 negatively regulates cardiac hypertrophy. [score:2]
0122509.g005 Fig 5 miR-185 negatively regulates the activity of CaMKIIδ in NRVMs. [score:2]
Then, human embryonic kidney (HEK)-293 cells were transfected using Lipofectamin LTX (Invitrogen) with 0.5 μg of the pmirGLO chimeric plasmid containing wild-type (WT) or mutant 3′-UTR along with the NC or miR-185 mimic (Dharmacon) at a final concentration of 15 nmol/L. [score:1]
Among the 18 GSA-identified cardiac hypertrophy -associated miRNAs, we selected miR-185 for further studies. [score:1]
While Nfatc3 harbors a single binding site for miR-185 in the 3′-UTR (Fig. 3C), there are multiple putative binding sites in the 3′-UTRs of Camk2d and Ncx1 in mouse (Fig. 3B and 3D). [score:1]
The mutant constructs were generated by introducing mutations into the putative miR-185 -binding sites by standard overlap PCR using mutagenic primers. [score:1]
Similar to the studies described above, in our studies miR-185 blunted cardiomyocyte hypertrophy (Figs. 1A-1D). [score:1]
HEK-293 cells were transfected with miR-185 in addition to the reporter constructs with WT or mutated 3′-UTR. [score:1]
The expression of the mRNAs was normalized to 18S rRNA and the level of miR-185 was normalized to U6 small RNA using the Hs_RNU6B_2 miScript Primer Assay (Qiagen). [score:1]
We attempted to verify the effects of these six miRNAs (miR-185, miR-139–5p, miR-374, miR-324–5p, miR-153, and miR-141) on myocardial hypertrophy. [score:1]
We also found that the level of miR-185 is approximately 2 fold higher in cardiomyocytes than cardiac fibroblasts, emphasizing the possible involvement of miR-185 in cardiomyocyte hypertrophy (Figure D in S1 File). [score:1]
miR-185 is encoded within an intron of the Tango2 gene (also known as T10) in the 22q11.2 region. [score:1]
To determine the level of miR-185 during the progression of cardiac hypertrophy, we carried out analysis. [score:1]
To investigate the role of miR-185 in cardiac hypertrophy, we transfected NRVMs with miRNA mimic or inhibitor of miR-185, followed by ET-1 stimulation. [score:1]
Similar anti-hypertrophic effects were observed when NRVMs were stimulated with other hypertrophic agents, such as isoproterenol (ISO, 10 μM) and phenylephrine (PE, 100 μM), after transfection of miR-185. [score:1]
miR-185 modulates CaMKIIδ activity in vitro. [score:1]
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[+] score: 114
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-181b-1, rno-mir-181b-2
To determine the effect of induced expression of miR-185 on the expression of SREBF1, COL1A1 and a-SMA in HSC cells, we determined the levels of SREBF1, COL1A1 and a-SMA in HSC cells when over -expressing miR-185 mimic or its inhibitor. [score:9]
Therefore, inhibition of SREBF1 expression following overexpression of miR-185 might be a mechanism associated with the increases in COL1A1 and a-SMA levels during liver fibrosis. [score:7]
Inhibitor, miRNA-185 inhibitor. [score:5]
These results suggested that miR-185 decreased SREBF1 expression and increased COL1A1 and a-SMA expression in HSC cells. [score:5]
miR-185 over -expression resulted in increased expression of COL1A1 and a-SMA genes in HSC cells. [score:5]
Furthermore, miR-185 targets SREBF1, and increases expression of COL1A1 and a-SMA genes that are involved in liver fibrosis. [score:5]
In the current study, we found that miR-185 mimic inhibits SREBF1 expression and increases COL1A1 and a-SMA levels in HSC cells. [score:5]
Circulating miR-185 is up-regulated in both the dimethylnitrosamine(DMN) and bile duct ligation(BDL) rat mo dels. [score:4]
We found that miR-185 is significantly up-regulated in blood specimens from both HBV-related liver fibrosis patients and rats with liver fibrosis. [score:4]
We found that SREBF1 contained sites that were potentially targeted by miR-185 (Fig. 5A). [score:3]
Elevated liver miR-185 expression blood and livers of patients with HBV-infected liver fibrosis. [score:3]
miR-185 targeted SREBF1 gene and changed COL1A1 and a-SMA mRNA and protein levels in HSC cells. [score:3]
In our current study, we have found that the expression of miR-185 is progressively elevated with aggravation of fibrosis. [score:3]
Since the samples we collected were blood samples from HBV liver disease patients, miR-185 is also as a biomarker for early diagnosis of HBV-related liver fibrosis. [score:3]
The miRNA mimics (ago-miR-185-5p), inhibitors (antago-miR-185-5p), and negative controls of miR-185-5p were purchased from RiboBio (RiboBio, Guangzhou, China). [score:3]
293T cells were transfected with reporter genes and miR-185 mimics and its inhibitors. [score:3]
The results confirmed that SREBF1 was the target of miR-185. [score:3]
To validate this finding, we performed a luciferase reporter gene assay with the human embryonic kidney cell line 293T, using constructs containing SREBF1 wild type or mutant sequences potentially targeted by miR-185 (Fig. 5B). [score:2]
The efficiency of diagnosis associated with the detection of miR-185 levels is greater than that of serum -based or imaging methods, which demonstrate lower specificity and sensitivity in the early diagnosis of liver fibrosis 2 21. [score:1]
The results showed that the luciferase activity of the wild-type construct was significantly decreased by miR-185, but not by the mutant constructs (Fig. 5C). [score:1]
Diagnosis of liver fibrosis in patients with HBV infection using circulating miR-185 levels. [score:1]
Therefore, circulating miR-185 levels may be a potential biomarker for the early-stage diagnosis of HBV-related liver fibrosis. [score:1]
The miR-185 levels can differentiate between early-staged and advanced-staged liver fibrosis in healthy controls with high specificity, sensitivity, and likelihood ratio. [score:1]
The results showed that an area under the ROC curve (AUC) of 0.8500 (95% CI: 0.7274–0.9726, P = 0.0001) was observed for the miR-185 levels in the early-stage liver fibrosis. [score:1]
Since liver fibrosis can progress to HCC, we speculate that there is an elevation in miR185 levels upon transition from liver fibrosis to HCC. [score:1]
Most interestingly, the magnitude of the circulating miR-185 induction was dependent on the stages of fibrosis in DMN -induced liver fibrosis rat mo dels (Fig. 1B,C). [score:1]
In situ hybridization data show that miR-185 is deposited in collagen deposition regions during advanced liver fibrosis, indicating that miR-185 levels may be induced in activated HSC cells. [score:1]
This confirms that miR-185 is a promising indicator for liver fibrosis. [score:1]
Mimic, miRNA-185 mimics. [score:1]
How to cite this article: Li, B. -b et al. Potentials of the elevated circulating miR-185 level as a biomarker for early diagnosis of HBV-related liver fibrosis. [score:1]
The increases in the liver miR-185 levels were associated with collagen deposition. [score:1]
These results suggested the circulating miR-185 levels could be a potential marker for the pathogenesis and progression of liver fibrosis. [score:1]
ISH was performed using the miR-185-5p locked nucleic acid probe (5′-digoxigenin-UGGAGAGAAAGGCAGUUCCUGA-3′-digoxigenin) and the microRNA ISH Optimi-zation Kit (Exiqon, Vedbaek, Denmark) according to the manufacturer’s instructions. [score:1]
Blood miR-185 levels in rats with liver fibrosis induced by DMN and BDL. [score:1]
Circulating miR-185 levels were correlated with progression of liver fibrosis but not with viral loads in HBV-infected patients. [score:1]
The results suggested that the circulating miR-185 levels were useful in diagnosing liver fibrosis in patients with HBV infection with high specificity, sensitivity, and likelihood ratio. [score:1]
To determine whether blood miR-185 levels are correlated with HBV viral loads, we analyzed correlation using samples from 24 HBV-infected patients with advanced-stage (F3-4) liver fibrosis. [score:1]
The magnitude of increases in the miR-185 levels is correlated with the progressive stages of liver fibrosis but not with different viral loads in HBV-infected patients. [score:1]
The relative miR-185 levels were determined using qRT-PCR. [score:1]
Using linear regression and correlation analysis, we found that circulating miR-185 levels were positively correlated with fibrosis stages (Rho = 0.542, p < 0.001; Fig. 3A). [score:1]
We speculate that increased miR-185 levels in the blood may be due to the increased release of miR-185 from the activated HSC cells. [score:1]
Notably, the miR-185 levels can discriminate early-stage of HBV-related liver fibrosis from the healthy controls with high specificity (95.24%), sensitivity (75%), and likelihood ratio (15.75) using ROC analysis (Fig. 4A). [score:1]
miR-185 mimic increased COL1A1 mRNA levels but had no obvious effect on a-SMA mRNA levels in HSC cells (Fig. 5D). [score:1]
The results suggested that miR-185 blood levels were increased in HBV-infected patients with liver fibrosis. [score:1]
To determine whether the miR-185 levels are correlated with the progression of liver fibrosis, we performed analysis of correlation between the miR-185 levels and the stages of liver fibrosis in 57 HBV-infected patients who underwent liver biopsy. [score:1]
Using linear regression and correlation analysis, we found that there was no correlation between circulating miR-185 levels and HBV viral load (Rho = −0.075, p = 0.726; Fig. 3B). [score:1]
In conclusion, miR-185 levels can be used not only for the diagnosis of early-stage liver fibrosis but also as a potential biomarker for follow-up monitoring and assessment after treatment. [score:1]
The results showed that miR-185 mimic decreased SREBF1 mRNA and protein levels in HSC cells (Fig. 5D,E). [score:1]
We found that miR-185 levels in patients with HBV-related fibrosis were significantly higher in early-stage fibrosis (fold-changes = 1.65, p = 0.0001) and advanced-stage fibrosis (fold-changes = 2.96, P < 0.0001) than those in the healthy control group (Fig. 2A). [score:1]
Moreover, miR-185 levels in advanced-stage fibrosis yielded an AUC of 0.9395 (95% CI: 0.8725-1.006, P < 0.0001), which could be used to discriminate advanced-stage fibrosis from healthy volunteers with a higher specificity (95.24%) and sensitivity (87.5%) (likelihood ratio 18.37) (Fig. 4B). [score:1]
Our study, indicates that miR-185 levels might be used as a complemental diagnostic approach for the clinical pathological monitoring of early-stage liver fibrosis. [score:1]
Circulating miR-185 levels are correlated with the progression of liver fibrosis but not HBV-DNA loads in patients. [score:1]
Circulating miR-185 levels are elevated in patients with liver fibrosis in a stage -dependent manner. [score:1]
Interestingly, Wen and Han, et al. 20 found that HCC is independently associated with an increase in miR-185 20. miR-185 levels are increased in both liver fibrosis and HCC. [score:1]
Our data confirm that circulating miR-185 is a potential biomarker for liver fibrosis. [score:1]
After dehydration, the slides were incubated with a 40 nmol/L miR-185-5p probe at 50 °C for 120 min, followed by stringent washes with 5X standard saline citrate, 1X standard saline citrate, and 0.2X standard saline citrate buffers at 50 °C, and finally incubated with digoxigenin blocking reagent (Roche, Mannheim, Germany). [score:1]
miR-185 mimic significantly elevated COL1A1 and a-SMA protein levels in the HSC cells (Fig. 5E). [score:1]
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[+] score: 23
While the role of miR-450a on the regulation of endocrine function or in diabetes is not clear to date, miR-185 plays an important role in the regulation of insulin secretion and β cell growth via targeting suppressor of cytokine signaling 3 (SOCS3) [27]. [score:7]
Based on previous work, the expression of the two increased miRNA species miR-375 and miR-210 and the three decreased miRNAs, miR-203, miR-185 and miR-450a, is involved in the regulation of insulin secretion and pancreatic β cell function [11, 26, 27, 28]. [score:4]
However, miR-185 can also block cardiac hypertrophy signaling and was discussed as a target for heart failure treatment [33]. [score:3]
Furthermore, our study showed significant alteration in the circulating level of miR-185 and miR-450a during the progression of the disease. [score:3]
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
A significantly decreased miR-185 blood level was detected in patients with diabetes and in pancreatic islets of diabetic mouse mo dels [27]. [score:1]
Further elucidation of the role of miR-185 in humans is required. [score:1]
Furthermore, miR-185 has been identified in several cancer types and may therefore not be a specific marker. [score:1]
These findings point towards a functional role of miR-185 in diabetes progression. [score:1]
Diminution in circulating levels was detected for miR-140, miR-151-3p, miR-185, miR-203, miR-434-3p and miR-450a (Figure 5). [score:1]
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[+] score: 20
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]
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[+] score: 19
For example, the oncogenic miR-185 was significantly up-regulated in ccRCC and anti-correlated with the tumor suppressor gene PTEN, suggesting that its gain of function shuts down PTEN in ccRCC. [score:6]
Another identified target of miR-185 was PTPN13 (also a predicted miR-185 target in miRBase: http://microrna. [score:5]
For instance, loss of miR-149, miR-200c and mir-141 causes gain of function of oncogenes (KCNMA1, LOX), VEGFA and SEMA6A respectively and increased levels of miR-142-3p, miR-185, mir-34a, miR-224, miR-21 cause loss of function of tumor suppressors LRRC2, PTPN13, SFRP1, ERBB4, and (SLC12A1, TCF21) respectively. [score:3]
KCNJ16, member of the potassium channel subfamily of membrane proteins, was also identified as a target of miR-185. [score:3]
As the p-values in Figure 4 indicate, we validate a strong anti-correlation signature between mRNA levels of (KCNMA1, LOX), VEGF, SEMA6A, (LRRC2, PTPN13), SFRP1, ERBB4, SLC12A1 and TCF21, and their identified regulators: miR-149, miR-200c, mir-141, miR-142-3p, miR-185, mir-34a, miR-224 and miR-21 respectively. [score:2]
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[+] score: 18
The unique miRNA expression patterns distinguishing the ASH group from the control group were composed of six downregulated (miR-199a-3p, miR-214, miR-93, miR-146a, miR-191 and let-7b) and six upregulated (miR-129, miR-490, miR-21, miR-503, miR-183 and miR-185) miRNAs. [score:9]
As expected, several miRNAs, including miR-185 (10) and miR-21 (12), which were identified to be differentially expressed in ALD patients by microarray, were also identified as differentially expressed in ALD in this animal mo del study. [score:5]
Further microRNA-gene networks indicated that the key microRNAs were Homo sapiens (hsa)-miR-570, hsa-miR-122, hsa-miR-34b, hsa-miR-29c, hsa-miR-922 and hsa-miR-185, which negatively regulated ~79 downstream target genes to modulate hepatocyte immune response, inflammatory response and glutathione metabolism (10). [score:4]
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[+] score: 18
Overexpression of miR-223 decreased the levels of GluR2 and NR2B, inhibited NMDA -induced calcium influx in hippocampal neurons, and protected the brain from neuronal cell death following transient global ischemia and excitotoxic injury[64] Rno-miR-185 miR-185 has been associated with inflammatory responses during brain ischemic stroke in mice and may provide underlying target for prevention and treatment of stroke[65] Rno-miR-329 Inhibition of miR-329 increased neovascularization and blood flow recovery after ischemia in mice subjected to double femoral artery ligation[60] Rno-miR-138hypoxia -induced miR-138 is an essential mediator of endothelial cell dysfunction via targeting S100A1 Ca [2+] sensor[81] We showed that transcription factors, Maf, Creb1 and Stat1, were the 3 principal hubs with high connectivity in the early phase IR-injury regulatory network, whereas Stat1, Lef1 and Bcl6 were the 3 principal hubs in the late phase IR-injury network. [score:12]
For example, the top three miRNA-hubs in the early IR-injury regulatory network were rno-miR-495, rno-miR-214 and rno-miR-298, whereas rno-miR-873, rno-miR-223 and rno-miR-185 were hubs observed at the late phase post-IR injury. [score:2]
MiR-185 has been associated with inflammatory responses during brain ischemic stroke in mice and may provide underlying target for prevention and treatment of stroke [65]. [score:2]
We found that in the late phase of post-IR injury rno-miR-185 participates in four different loop-motifs (indicated by the thicker edges in Figure  6E) and these loop motifs are part of the sub-network linked to inflammatory responses. [score:1]
The thicker edges highlight the loop motifs that involve rno-miR-185. [score:1]
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[+] score: 10
miRNAs such as miR-133a, miR-185, miR-152, miR-34a and miR-342 which were reported to show increased expression were also up-regulated in our rat mo del. [score:6]
Nonetheless, the authors identified a pool of dysregulated miRNAs (∼50 miRNAs) in which some of them such as miR-144, miR-106b, miR-185, miR-30e, miR-589, miR-665 and many more showed similarities in expression as observed in our study (either humans/animals or both). [score:4]
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[+] score: 7
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
These miRNAs showed high representation in renal inflammation and nephritis pathways, and included miR-214, miR-130b, miR-150, miR-223, miR-142-5p, miR-185, and miR-296*. [score:1]
These six miRNAs are miR-130b, miR-296*, miR-223, miR-142-5p, miR-185, and miR-150. [score:1]
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10
[+] score: 7
The results showed that 14 miRNAs (miR-30a-5p, miR-30e-5p, miR-425-5p, miR-142-3p, miR-191a-3p, miR-215, miR-29b-3p, miR-30b-5p, miR-26a-5p, miR-345-5p, miR-361-5p, miR-185-5p, miR-103-3p) were down-regulated but no miRNA was up-regulated among above three altered miRNAs from microarray in OVX serum by normalizing to miR-25-3p (Fig. 3b). [score:7]
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[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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12
[+] score: 3
Among these aberrant miRNAs, ten miRs (miR-183-3p, miR-34c-3p, miR-200b, miR-466c, miR-465-3p, miR-185-3p, miR-320a, miR-493-5p, miR-181b-5p and miR-21-5p) were reported to be differentially expressed at both 12 and 48 h after IR. [score:3]
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[+] score: 2
Relative expression levels of the selected miRNAs and mRNAs were depicted in Figure 3. Consistent with the microarray data, real-time PCR confirmed that, compared with controls, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, and rno-miR-351-5p were significantly increased, while rno-miR-192-3p, rno-miR-194-5p, rno-miR-29c-3p, rno-miR-185-5p, and rno-miR-30c-5p were significantly decreased in stone-forming rat kidneys. [score:2]
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[+] score: 1
The involvement of microRNAs in major depression, suicidal behavior, and related disorders: a focus on miR-185 and miR-491–3p. [score:1]
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