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35 publications mentioning rno-mir-192

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-192. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 125
The miR-217 is known to be involved in increased collagen production and the progression of diabetic nephropathy through the down-regulation of PTEN and the subsequent activation of Akt kinase, and similar Akt up-regulation can be achieved by TGF-β -induced miR-192 18. miR-377 is thought to regulate the expression of fibronectin, another ECM protein that is up-regulated in diabetic nephropathy. [score:13]
To test our hypothesis that Taxol inhibits renal fibrosis through reduction of miR-192 levels, which down-regulate ECM protein expression, miRNA in vitro experiments were carried out. [score:8]
Taxol down-regulated miR-192, miR-217 and miR-377 in remnant kidney, while it up-regulated miR-15a by microarray (Figure 5B, C) and real-time PCR analyses (Figure 5D). [score:7]
In kidney, miRs have been reported to play a role in podocyte development 14– 16, the pathogenesis of diabetic nephropathy 17– 19 and polycystic kidney disease 20. miR-192, miR-217 and miR-377 have been described to be up-regulated in diabetic mouse and mesangial cells treated with TGF-β or exposure to high-glucose ambience 17– 19. [score:7]
They also reported that TGF-β1 -induced miR-192 up-regulation in mesangial cells increased the expression of COL(I)A2 by down -regulating Zeb2, an E-box repressor 17. [score:7]
The in vitro observations that miR-192 increases collagen expression, which is down-regulated by Taxol and also in the renal cortices of rat remnant kidney in vivo, underscores the significance of miR-192 among the three miRs in the pathobiology of interstitial fibrosis in this mo del. [score:6]
As expected, the tubular epithelial cells over -expressing miR-192 mimic or treated by TGF-β1 had significantly increased expression of not only miR-192 but also COL(I)A1 and COL(IV)A2. [score:5]
The central mechanism seems to be that Taxol interferes in the TGF-β1 -induced downstream signalling events, which include blockade of Smad2/3 activation and inhibition of miRNA-192, with a net result of decreased expression of collagen both in vitro and in vivo systems. [score:5]
As shown in Figure 5G, the antibody directed against Smad3 immunoprecipitated the DNA fragments from NRK52E cells containing the potential binding sites of SBS1and SBS2, supporting the hypothesis that Smad3 can physically interact with the miR-192 promoter region, and their activities were remarkably suppressed by Taxol. [score:4]
Kato et al and Chung et al have reported that miR-192 was up-regulated in cultured mesangial and tubular cells treated with TGF-β1 18, 46. [score:4]
Since the most remarkable changes were seen in miR-192, the studies were extended and its expression was also assessed by northern blot analyses in the remnant kidney. [score:3]
On the other hand, transfection of antisense miR-192 reduced the gene and protein expression induced by TGF-β1. [score:3]
In the remnant kidney, the miR-192 expression increases notably by 4 weeks, and by 8 weeks a steep increase was observed. [score:3]
[Δ] p < 0.05 versus Mock group; [#] p < 0.05 versus TGF-β1 group; [▴] p < 0.05 versus miR192 group (n = 6) Figure 7Effect of miR192 transfection on COL(I)A1 and COL(IV)A2 expression in NRK52E cells, as assessed by immunofluorescence microscopy. [score:3]
An increase in the cellular expression of COL(I)A1 and COL(IV)A2 was observed with the transfection of miR-192, and it was remarkably reduced with Taxol treatment (Figure 7A, B). [score:3]
Taxol treatment reduced the expression of three miRNAs, especially that of miR192, as assessed by microarray analyses. [score:3]
They observed a 70% drop in miR-192 expression with serum deprivation, which was essentially reversed by TGF-β. [score:3]
[Δ] p < 0.05 versus Mock group; [#] p < 0.05 versus TGF-β1 group; [▴] p < 0.05 versus miR192 group (n = 6) Figure 7Effect of miR192 transfection on COL(I)A1 and COL(IV)A2 expression in NRK52E cells, as assessed by immunofluorescence microscopy. [score:3]
By using ChIP assays, we demonstrated that an antibody directed against Smad3 could successfully immunoprecipitate DNA fragments containing the potential Smad3 -binding sites, thus supporting the Chung et al 46 findings that Smad3 could physically interact with the promoter region of miR-192, and that Taxol is capable of suppressing Smad3 -mediated miR-192 transcriptional activity. [score:3]
The role of miR-192 in kidney diseases is still controversial. [score:3]
miR-192 expression increased significantly at 4 and 8 weeks following surgery and was substantially reduced with Taxol treatment. [score:3]
Figure 6Effect of miR192 transfection on ILK, COL(I)A1, COL(IV)A2 and α-SMA expression in NRK52E cells. [score:3]
Modulation of COL(I)A1 and COL(IV)A2 expression by miR-192 and TGF-β1 in NRK52E renal tubular epithelial cells. [score:3]
The expressions of three miRNAs, miR-217, miR-192 and miR-377, were found to be consistently high, and they were decreased with low-dose paclitaxel treatment in all three different biological samples, ie cortices, isolated tubular cells and NRK52E cells. [score:3]
Also, the expressions of COL(I)A1, COL(IV)A2 and miR192, but not of ILK and α-SMA, were increased in miR-192 -transfected NRK52E cells compared to Mock (p < 0.05, n = 6). [score:2]
The miR-192 -transfected NRK52E cells had a significantly increased expression of both collagen I and collagen IV compared with the Mock group (p < 0.05, n = 6). [score:2]
The transfection of AS-mIR-192 caused a remarkable reduction in the expression of COL(I)A1 and COL(IV)A2 in TGF-β1 -treated cells, while that of ILK and α-SMA were unaltered. [score:2]
The miR-192 transfection led to a two- to three-fold higher expression of COL(I)A1 and COL(IV)A2 compared to the treatment with TGF-β1, while that of ILK and α-SMA were indistinguishable (Figure 6A). [score:2]
These data indicate that miR-192 and ILK may have independent actions that converge at the downstream events related to TGF-β/Smad3 signalling in the development of renal fibrosis. [score:2]
[#] p < 0.05 versus Mock group (n = 6); [▴] p < 0.05 versus miR192 group (p < 0.05, n = 6) Rats that had undergone subtotal nephrectomy developed hypertension at the end of the second week and it was not relieved by the paclitaxel (Taxol) treatment (Figure 1A). [score:1]
In the Wang et al experiments, under reduced serum conditions the TGF-β1 treatment resulted in a decrease rather than increase in miR-192 levels. [score:1]
Kato et al and Chung et al 18, 46 also reported an increase in miR-192 in the diabetic kidney, UUO and the rat 5/6 nephrectomy mo del, in contrast to the Wang et al studies in diabetic kidneys, where miR-192 was decreased. [score:1]
Low-molecular weight RNA (50 µg) was run on a denaturing 10% polyacrylamide gel, transferred to PVDF membrane (Amersham/GE Healthcare, Piscataway, NJ, USA), subjected to UV light irradiation for 4 min and baked at 80 °C for 1 h. The locked nucleic acid (LNA) -modified miR-192 oligonucleotide probe (5′-CTGACCTATGAATTGACAGCC-3′) was purchased from Exiquon (Woburn, MA, USA). [score:1]
The effects accentuated by TGF-β1 were abolished with the AS-miR-192 treatment (p < 0.05, n = 6). [score:1]
By employing Lipofectamine 2000, subconfluent cells were then transfected with four different miRs: hsa-miR-192 mimic (50 n m); negative control (miR-neg; Sigma); antisense-miR-192 (400 n m); or control antisense-miR (Genepharma, Shanghai, China). [score:1]
In conclusion, low-dose Taxol significantly improves kidney functions and attenuates renal injury following subtotal renal ablation in rats by modulating mir-192 biology, which seems to be intimately interlinked with TGF-β/Smad signalling. [score:1]
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2
[+] score: 89
Other miRNAs from this paper: rno-mir-21, rno-mir-126a, rno-mir-210, rno-mir-126b, rno-mir-155
Roy et al. [34] recently found that tumor necrosis factor alpha (TNF-α) was an upstream regulator of miR-192 in acute liver injury and confirmed a protective effect of downregulation of miR-192 in hepatocytes through Zeb2. [score:5]
Plasma miR-192 expression started increasing at 3 h and peaked at 12 h, while kidney miR-192 expression started decreasing at 6 h and remained at a low level for 7 days after reperfusion. [score:5]
Plasma miR-192 expression was induced in a time -dependent manner after IRI in rats and patients with AKI after cardiac surgery, comparably to the kidney injury development and recovery process, and may be useful for the detection of AKI. [score:4]
Previous studies suggest that miR-192 was linked to both G1 and G2/M cell cycle arrest in other contexts [29, 30] and was frequently downregulated in colorectal cancer, renal childhood neoplasms and multiple myeloma [31– 33]. [score:4]
A previous study indicated that plasma miR-192 was upregulated at 6 h after reperfusion in IRI rats [20]. [score:4]
Moreover, miR-192 expression pattern in humans and rats seems to be different. [score:3]
Our study showed dynamic changes of miR-192 expression in the plasma and kidney tissues of IRI rats. [score:3]
In the time-course study, miR-192 expression in the plasma and kidney tissues of IRI rats varied in a time -dependent manner. [score:3]
a The miR-192 expression of patients [#] p < 0.05, [##] p < 0.01 versus prelevels; * p < 0.05 versus the non-AKI group; [@] p < 0.05 versus post 0 h. b The area under the ROC curve of post 2 h miR-192 Table 1 Plasma miR-192 levels of patients at different time points Non-AKI AKI p value (AKI vs. [score:3]
That might be due to some risk factors for AKI, such as diabetes, lupus nephritis, infection diseases and pre-existing cancer that were excluded in this study in case of all these confounding factors affected the analysis of miR-192 levels. [score:3]
Plasma miR-192 expression was elevated at 3 h after reperfusion, peaked at 12 h and returned to baseline at 3 day after reperfusion (Fig.   3d). [score:3]
Dynamic changes of plasma and kidney miR-192 expression in IRI rats. [score:3]
Moreover, the expression pattern of plasma miR-192 was discordant with that of kidney miR-192. [score:3]
Fig.  4Plasma miR-192 expression of patients in the AKI group varied over time and could predict AKI incidence after cardiac surgery. [score:3]
We further confirmed the expression of miR-192 in kidney tissues. [score:3]
WK, whole kidney, * p < 0.05, ** p < 0.01, *** p < 0.001 versus the sham group Among the identified miRNAs, miR-192 was preferentially expressed in the kidney and showed more than a threefold change. [score:3]
In the present study, we analyzed miR-192 expression levels in the plasma and kidney tissues from IRI rats after miRNA profiling and verified its changes in the plasma of patients after cardiac surgery at different time points to determine whether miR-192 can be used as a tool to detect IRI kidney injury. [score:3]
The expression pattern of miR-192 in the non-AKI group was similar to that of the patients with AKI, except that miR-192 levels decreased at 2 h, but was still higher than that before operation. [score:3]
In IRI rats, miR-192 expression was decreased by about 40% in the whole kidney, about 60% in the medulla and about 40% in the cortex, compared to the sham group (Fig.   2c). [score:2]
The expression of miR-192, a specific kidney-enriched miRNA, was assessed in both the plasma and kidney of IRI rats at different time points after kidney injury and compared to renal function and kidney histological changes. [score:2]
However, the time-course study showed significantly decreased levels of miR-192 in kidney tissues of IRI rats, with an initial decrease at 6 h and a continuous low level until 7 day after reperfusion (Fig.   3e). [score:1]
Small number of cases, mild clinical AKI and limited time points between 2 and 24 h after reperfusion may have reduced the diagnostic value of miR-192 in AKI. [score:1]
miR-192 Acute kidney injury Cardiac surgery microRNAs Ischemia–reperfusion injury Acute kidney injury (AKI) is one of the most common complications in patients with prolonged hospital stays, increasing medical costs and poor outcomes [1]. [score:1]
To investigate how early miR-192 was changed after renal IRI, we observed the dynamic expression of miR-192 in the plasma and kidney tissues of IRI rats. [score:1]
Although miR-192 level in the heart tissue is much lower than that in the kidney, investigators showed that hypoxia induced miR-192 expression and excretion in the sera of patients with post-acute myocardial infarction (AMI) [27]. [score:1]
Therefore, we chose miR-192 for further validation. [score:1]
Plasma (d) and renal tissue (e) miR-192 levels in the IRI and sham groups at different time points. [score:1]
As shown in Fig.   4a and Table  1, plasma miR-192 levels increased rapidly at 0 h after admission to the ICU and were stable between 0 and 2 h after surgery in patients who developed AKI. [score:1]
The area under the ROC curve (AUC-ROC) was 0.673 (95% CI: 0.540–0.806, p = 0.014) for plasma miR-192 at 2 h after ICU admission, indicating that plasma miR-192 can be an early marker for the detection of established AKI. [score:1]
Circulating levels of miR-192 increased in patients after cardiac surgery. [score:1]
In miRNA PCR array and miR-192 validation study, nine rats in each group were euthanized after 24 h of reperfusion. [score:1]
Firstly, the plasma level of miR-192 in non-AKI patients at the time of admission to ICU (0 h) was also significantly higher than the preoperation level. [score:1]
b Plasma and c renal tissue miR-192 levels in the IRI and sham groups. [score:1]
However, rat plasma miR-192 began to increase at 3 h after reperfusion. [score:1]
Real-time PCR showed that miR-192 levels increased by fourfold in the plasma and decreased by about 40% in the kidney of IRI rats. [score:1]
Plasma miR-192 level in patients with AKI increased at the time of ICU admission, was stable for 2 h and decreased after 24 h. AUC-ROC was 0.673 (95% CI: 0.540–0.806, p = 0.014). [score:1]
In addition, only one time point difference in the level of miR-192 was observed and the AUC was not very high. [score:1]
Fig.  3Time course of the IRI -induced dynamic kidney injury and changes of miR-192 in the plasma and kidney tissues of IRI rats. [score:1]
In addition, we observed dynamic changes of plasma miR-192 levels in patients undergoing cardiac surgery and provided a time window for clinical testing. [score:1]
Thus, miR-192 may reflect kidney IRI. [score:1]
The level of plasma miR-192 in AKI patients was significantly higher than that of non-AKI patients at 2 h after ICU admission. [score:1]
In the clinical study, plasma miR-192 at 2 h after ICU admission presented a modest predictive value for the diagnosis of AKI. [score:1]
In summary, this study showed dynamic changes of plasma and kidney miR-192 levels in AKI and plasma miR-192 might be a predictor for ischemic AKI. [score:1]
ROC curve analysis showed that miR-192 could be used to diagnose AKI (Fig.   4b). [score:1]
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3
[+] score: 54
However, opposite results were shown in a kidney disease mo del of obstructive nephropathy, in which over -expression of Smad7 inhibited the expression of miR-192 and resulted in suppression of renal fibrosis [41]. [score:11]
It was found that 8 miRNAs were significantly and consistently down-regulated in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b), and within which miR-192, miR-194 and miR-200b were also down-regulated in the normal saline group (Table  3). [score:7]
The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. [score:7]
The results demonstrated that in the hypertonic dialysate group, miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were all significantly down-regulated whereas miR-122 was highly up-regulated (all P <0.05) (Figure  3). [score:7]
Cg Down-regulated Fold-change Fold-change Fold-change rno-miR-310.37 [*] 0.42 [*] / rno-miR-1000.45 [*] 0.40 [*] / rno-miR-930.45 [*] 0.48 [*] / rno-miR-1520.38 [*] 0.40 [*] / rno-miR-4970.33 [*] 0.44 [*] / rno-miR-192 /0.24 [*] 0.28 [*] rno-miR-194 /0.14 [*] 0.12 [*] rno-miR-200b /0.19 [*] 0.27 [*] Up-regulated Fold-change Fold-change Fold-change rno-miR-1223.87 [*] 2.49 [*] / *indicates significant difference between the two groups. [score:7]
Compared with the control and saline groups, both miRNA microarray and real-time PCR analyses demonstrated that miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were significantly down-regulated, and miR-122 was highly up-regulated in the hypertonic dialysate group. [score:6]
Decreased expression of miR-192 was detected in patients with established diabetic nephropathy, and its expression level correlated with the degree of tubulointerstitial fibrosis [40]. [score:5]
Further studies are needed to elucidate how miR-192 exhibits its inhibitory activity on peritoneal fibrosis. [score:3]
Taken together, these results suggest to us that the miRNA species identified in our miRNA screen (mir-31, mir-93, mir-192, mir-194 and mir-200b) may be critical in the process of mesothelial cell EMT and in the progression of peritoneal fibrosis. [score:1]
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4
[+] score: 54
Correspondingly, in the high glucose media, expression of miR-144 was found to be highest (3.605±0.21) accompanied by a down-regulation of IRS1 (−3.257±0.29), followed by miR-150 (2.904±0.19) and miR-192 (1.989±0.20) which are predicted to target GLUT4 (−2.604±0.25) and CBL (−4.672±0.31) and INSR (1.150±0.28) respectively. [score:8]
miR-29a, miR-144, miR-150, miR-192 and miR-320 showed an up-regulation from that of control samples whereas miR-30d, miR-146a and miR-182 showed down-regulation. [score:7]
miRNAs such as miR-144, miR-29a and miR-192 that were up-regulated in both IFG and T2D patients (Table S8) are predicted to target IRS1, AKT2 and INSR respectively. [score:6]
In contrast, miR-192 expression remained close to basal level in the IFG group while miR-144 showed a significant up-regulation against healthy controls but at a lower fold change compared to that in T2D (IFG: 1.385±0.14; T2D: 3.070±0.13). [score:5]
miR-144 and miR-192 were among the highly up-regulated miRNAs in T2D. [score:4]
In all five sources, miR-144, miR-150, miR-192, miR-29a and miR-320a were found to be highly up-regulated. [score:4]
miR-144, miR-146, miR-182 and miR-192 showed a lower expression compared to the other miRNAs in the three insulin target tissues as well as in the pancreas. [score:4]
Altered expression of miR-192 and miR-377 has also been reported in diabetic kidney glomeruli and diabetic nephropathy respectively [35], [36]. [score:3]
Besides miR-192 [35] and miR-29a [34] which have previously been shown to be implicated in diabetes, we have also observed an approximately linear relationship between miR-144 expression and increasing glycaemic status (from IFG to T2D). [score:3]
The eight miRNAs (miR-144, miR-146a, miR-150, mR-182, miR-192, miR-29a, miR-30d and miR-320) which were previously identified in the rat study showed similar expression in the patients' blood miRNAs. [score:3]
We have also identified eight important miRNAs (miR-144, miR-146a, miR-150, miR-182, miR-192, mir-29a, miR-30d and miR-320) that could participate in the regulation of insulin signaling as well as useful in distinguishing different stages of diabetes progression. [score:2]
Although our results were in conjunction with earlier studies which identified miR-192, miR-29a, miR-320 and miR-30d to be potential key players in the pathogenesis of T2D, we do observe differences in the recent study reported by Zampetaki et al [20]. [score:1]
Employing miRNA microarray and stem-loop real-time RT-PCR, we identify four novel miRNAs, miR-144, miR-146a, miR-150 and miR-182 in addition to four previously reported diabetes-related miRNAs, miR-192, miR-29a, miR-30d and miR-320a, as potential signature miRNAs that distinguished IFG and T2D. [score:1]
Association of miR-192 [35], miR-29a [34] and miR-320 [50], [51] in T2D has been reported in previous studies and our study also shows similar results. [score:1]
Predictions: miR-144/ IRS1; miR-146a/ PTPN1; miR-150/ GLUT4 and CBL; miR-182/ FOXO1; miR-192/ INSR; miR-30d/ INS; miR-29a and miR-320/ AKT2. [score:1]
Among these eight miRNAs, four of them namely miR-192 [35], miR-29a [34], miR-30d [49] and miR-320a [50], [51] had previously been reported in earlier studies and our results were consistent with them. [score:1]
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5
[+] score: 36
The negative correlation between the gene and microRNA expression suggests that the increased mRNA levels of growth factors (Egr1, Fgf2, and Fgf7) may be due to the downregulated expression of their regulating microRNAs (miR-192, miR-143). [score:9]
The presented data indicate that, among others, the activation takes place due to the opposed expression profile of genes and their regulating microRNAs at the site of inflammation (Figure 6); while the expression of all tested mesenchymal markers (Egr1, Fgf2, Fgf7, Jak2, Notch2, Hif1 α, Zeb2, Mmp9, Lox, and Vim) was significantly induced, microRNAs regulating their expression decreased (miR-192, miR-143, miR-375, miR-30a, miR-107, miR-200b, and miR-125a). [score:9]
It is known that miR-192 regulates the expression of Egr1 and Fgf2, while miR-143 is a known inhibitor of Fgf7 [20]. [score:6]
These data show that the expression of Zeb2 is de-repressed at the site of colonic inflammation due to the decreased expression of its microRNA regulators miR-200b and miR-192. [score:6]
It is important to note that miR-192, also known to regulate the expression of Zeb2 [28], exhibits similar expression profile as miR-200b (Figure 2(d)). [score:6]
[1 to 20 of 5 sentences]
6
[+] score: 25
0037395.g003 Figure 3(A) Serum miR-122 expression levels; (B) Serum miR-192 expression levels; (C) Serum miR-193 expression levels; (D) Biochemical parameter: serum ALT levels; (E) Biochemical parameter: serum AST levels. [score:7]
0037395.g004 Figure 4(A) Serum miR-122 expression levels; (B) Serum miR-192 expression levels; (C) Serum miR-193 expression levels; (D) Biochemical parameter: serum ALT levels; (E) Biochemical parameter: serum AST levels; The absolute concentrations of target miRNAs were calculated by referring to calibration curves developed with corresponding synthetic miRNA oligonucleotides. [score:7]
By individual TaqMan qRT-PCR analysis of dysregulated serum miRNAs uncovered by serum TLDA and dysregulated liver tissue miRNAs uncovered by microarray hybridization in primary screening, 6 serum miRNAs, including miR-122, miR-192, miR-193, miR-200a, miR-21 and miR-29c, exhibited a high correlation with primary screening results. [score:3]
Among this set of serum miRNAs, miR-122, miR-192 and miR-193 presented a significant change in both DILI mo del groups within the threshold of a fold change >10 and P-value<0.05 (Table 1). [score:1]
In the dose -dependent analysis of the serum miRNAs miR-122, miR-192 and miR-193, miR-122 showed extremely high sensitivity in both 2 DILI mo del groups (fold change >50.0), while serum biochemical parameters (e. g., ALT and AST) displayed only mild sensitivity (fold change <20.0) in the high-dose group. [score:1]
In the time -dependent analysis of the serum miRNAs miR-122, miR-192 and miR-193, all of these serum miRNAs exhibited an ascending trend 3 h after administration in both DILI mo del groups (fold change >2.0); while serum biochemical parameters (e. g., ALT and AST) remained at baseline levels (fold change <1.5). [score:1]
Beside, among the three serum miRNAs as potential diagnostic biomarker for DILI explored in rat mo dels in present study, miR-122 and miR-192 was also validated in plasma of mice mo dels by Wang et al. [27]. [score:1]
Previously, plasma miR-122 and miR-192 had been reported increased linearly from 1 to 3 hours and displayed dose -dependent manner after APAP overdosing in mice. [score:1]
The panel of aberrantly expressed serum miRNAs (miR-122, miR-192 and miR-193) all exhibited time- and dose -dependent characteristics. [score:1]
In summary, serum miR-122, miR-192 and miR-193 constitute a new panel for compound- and herb -induced liver injury diagnosis. [score:1]
Our results demonstrate that a new panel of serum miRNAs (miR-122, miR-192 and miR-193) could have the potential to serve as sensitive, specific and noninvasive biomarkers for the diagnosis of DILI. [score:1]
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7
[+] score: 24
Reduced expression of miR-192, miR-215 and miR-10b in liver samples of rat from fish oil group (Fig. 3B) resulted in a de-repression of their targets plasminogen activator inhibitor type 1 (Serpine1) and insulin-like grow factor 2 (Igf2), as both genes have predicted binding sites for these three miRNAs. [score:7]
Among the validated gene targets of some of these miRNAs, there is the insulin grown factor pathway (Igf-1r and Igf-1), which is targeted by miR-192 and miR-215 [33]. [score:5]
By contrast, miR-26b-5p, miR-199a-3p, miR-377–3p, miR-let-7f-5p, miR-200a-3p, miR-21–5p, miR-152–3p, and miR-192–5p expressions were repressed by SO diet consumption. [score:3]
Moreover, Igf2 and Serpine1 are among predicted targets of this family of miR-192/215. [score:3]
Igf2 and Serpine1 are targets of miR-192/215 and miR-10b family. [score:3]
Adult offspring of rats that were fed the FO diet during the first 12 days of pregnancy showed lower expression of miR-192 compared with SO, OO, LO, and PO diets. [score:2]
Likewise, we observed a decrease in the expression of several hepatic miRNAs, namely miR-192–5p, miR-10b-5p, miR-377–3p, and miR-215 after FO compared with OO and PO diets and miR-21–5p and mir-26b-5p after FO compared with PO diets. [score:1]
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8
[+] score: 21
Furthermore, the decreased expression of miR-192 seems to correlate directly with tubulointerstitial fibrosis and a low glomerular filtration rate, and TGF-β suppresses miR-192 expression in cultured proximal tubular cells [26]. [score:8]
On the other hand, miR-192 and miR-194 were highly expressed in the kidney and small intestine, and miR-449a was highly expressed in the lung (Figures 3(d) and 3(e)). [score:5]
miR-192 and miR-194 were highly expressed in the kidney and in the small intestine. [score:3]
The expression of miR-200a, miR-200b, miR-200c, miR-192, miR-194, and miR-449a was validated with real-time RT-PCR in rat tissues in order to discriminate the kidney from other tissues with a tubular structure. [score:3]
Consistently, the plasma concentrations of the miR-200 family members and miR-192 and miR-194 increased significantly. [score:1]
A significant increase in plasma miR-200a/b/c, miR-192, and miR-194 levels was observed in the AKI mo del. [score:1]
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9
[+] score: 19
Other miRNAs from this paper: rno-mir-141, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-429
Members of the miR-200 family and miR-192 act as protectors of the normal epithelial phenotype and are markedly downregulated in TGF-β -induced EMT [16], [17]– [21]. [score:4]
0071310.g009 Figure 9 Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
Expression of the miR-200 family and miR-192. [score:3]
Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
Expression Profile of the miR-200 Family and of miR-192 in Isolated Glomeruli. [score:3]
As miRNAs have been suggested as playing a key role in a variety of kidney diseases, we investigated the expression of the miR-200 family and miR-192 in isolated glomeruli from LP compared to NP offspring. [score:2]
Each cDNA of miRNA-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) and miR-192 was quantified by real-time quantitative PCR using ABI Prism 7900 Sequence Detection System (Life Technologies, USA). [score:1]
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10
[+] score: 18
Importantly, while the expression of certain miRNAs was found to overlap across the two different populations (i. e., miR-122, miR-192 and Let-7a) the expression of other miRNAs was found to be differentially regulated. [score:6]
The analysis shows that liver-enriched miRNAs [miR-122 (P = 0.007) and miR-192 (P = 0.03)] are up-regulated at day 2 after PHx and the levels are reduced to almost pre-PHx levels (i. e., day 0) at days 4 and 6 after PHx (Fig. 6, top row). [score:4]
We now show that administration of IL-6 to activated HSCs significantly down-regulates the level of several EV -associated miRNAs, including miR-192, -194, -150, -155 and -21 (Fig. 9b). [score:4]
It was found that the expression of miR-122 (P = 0.0001), miR-192 (P = 0.004), miR-194 (P = 0.03)] and Let-7a (P = 0.006) followed the same pattern as observed for vesicles -associated miRNAs (top rows in Figs 6 and 7), suggesting that these miRNAs do undergo comparable modulation in both fractions. [score:3]
Specifically, we found that the cytokines used in this study significantly increased levels of miR-122, miR-150, miR-21, miR-192 and miR-194 associated to EVs secreted from PCs. [score:1]
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[+] score: 14
Of the nine miRNAs in this IRI-specific expression signature, six showed differential expression in our study (four of which exhibited increasing expression with age, including miR-21, miR-146a, miR-192, and miR-194) (Figure  6). [score:7]
The miRNAs that showed highest expression during middle or young adult ages (15 and 21 weeks) were miR-192 and miR-194 (Figure  6B,H), both of which show steady increase in expression at early ages, that peak at 15 and 21 weeks of age, before decreasing at older ages. [score:5]
For example, anti-miR-192 has been used to decrease glomerular fibrosis in mouse mo dels of diabetic nephropathy [19]. [score:1]
For example, nine miRNAs (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805, and miR-194) have been identified in C57BL/6 mice as promising biomarkers of kidney injury after renal ischemia reperfusion injury (IRI) [15]. [score:1]
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In agreement, we showed that the expression of rno-miR-192, rno-miR-194, and rno-miR-499 was higher in the stone-forming group while their potential target gene chemokine receptor 2 (CCR2) was lower. [score:5]
Among these differentially expressed miRNAs, rno-miR-130b-3p, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, rno-miR-351-5p, and rno-miR-21-3p had the largest positive fold changes, while rno-miR-335, rno-miR-192-3p, rno-miR-194-5p, rno-miR-192-5p, rno-miR-499-5p, and rno-miR-210-3p had the largest negative fold changes (Table 1). [score:3]
Therefore, we proposed that, in the process of kidney stone formation, the overexpression of CCR2 mediated by relevant miRNAs, such as rno-miR-192, rno-miR-194, and rno-miR-499, would induce the inflammation and damage to the renal tubular epithelial cells and promote nephrolithiasis. [score:3]
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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miRNAs have been associated with and put forth as putative biomarkers of human disease, including hepatitis C (miR-122) [6], cardiovascular diseases (miR-192) [7] and various types of cancers [8]. [score:5]
In contrast, the findings presented in this dog atlas show that cfa-miR-192 was expressed at relatively high levels (>650 RPM) in all tissues. [score:3]
Kidney enriched miR-10a and miR-192 were previously identified as potential circulating biomarkers of renal injury in rats [48], however miR-192 had high expression in multiple dog tissues and was not identified as kidney enriched in the current study. [score:3]
Others have reported miR-192 as a liver specific biomarker in multiple species [9, 20]. [score:1]
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Almost all the up-regulated miRNAs (22 our of 25 miRNAs) such as miR-122, miR-192, miR-685, miR-193, and miR-29c were also up-regulated in our rat mo del, suggesting that common plasma miRNAs seem to be up-regulated in APAP -induced liver injury independent of species. [score:10]
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and 24 miRNAs were significantly downregulated (rno-miR-192-3p, rno-miR-192-5p, rno-miR-33-5p, rno-miR-196c-3p, etc. ) [score:4]
miR-141, miR-200a, miR-192, and miR-205 are upregulated in patients with hypertensive glomerulosclerosis [43]. [score:4]
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The expression of tissue specific miRNAs is often regulated at the transcription level by tissue specific transcription factors (for examples, miR-122a by HNF4, miR-192 and miR-194 by HNF1 [8], [9]. [score:4]
Similarly, genes encoding for miR-192 and miR-194 are clustered on chromosome 1, and could explain their coordinated increase in expression (Table 2). [score:3]
Similarly, the binding site of a liver specific transcription factor HNF-1 can be predicted in the 5′ upstream region of miR-122a, miR-192 and miR-194-2 [9], [27], [36]. [score:1]
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Next, the expression of four endogenous miRNAs (miR-122, miR-192, miR-21 and miR-16) was analyzed by qPCR, showing that the detection of the analyzed targets sequence is linear (as shown by the linear regression R [2]). [score:5]
Microarray analysis identified a panel of miRNAs, which are either highly expressed in the heart (miR-1, miR-133a and miR-16) or in the liver (miR-122, miR-192 and miR-194) or invariant (miR-21; Supplementary Figure 1a). [score:3]
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IsomiRs of miR-192-5p display more expanded or restricted expression with respect to tissues. [score:3]
IsomiRs in other tissues such as isomiRs of miR-215 in the intestine (Additional file 11: Figure S3), miR-192-5p in the liver (Additional file 12: Figure S4) and miR-3473f-pre in the testis (Additional file 13: Figure S5 and Additional file 14: Figure S6) display similar isomiR expression. [score:3]
IsomiRs of miR-192-5p in the liver. [score:1]
Additionally, miR-122 and liver enriched miR-192 were increased in the serum of patients who had acetaminophen induced hepatotoxicity demonstrating the potential for these miRNAs to be used as both preclinical and clinical biomarkers for liver injury [24]. [score:1]
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In a study conducted on HeLa cell lines, results showed that the miR-192/194 cluster directly regulates the entire Period gene family, with increased expression of the miR192/194 tandem causing lowered expression of the Period genes and a shortening of the circadian cycle [11]. [score:7]
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A recent study demonstrates that AA treatment altered a number of miRNAs in proximal tubular epithelial cells such as up-regulation of miR-192, miR-194, miR-450a, and miR-542. [score:4]
miR-192 mediated DNA damage response and recapitulated G2/M arrest via repression of murine double-minute 2, a negative regulator of P53 [40]. [score:2]
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Other miRNAs from this paper: rno-mir-27a, rno-mir-29c-1, rno-mir-377, rno-mir-29c-2
For instance, miR-192 levels are significantly increased in diabetic glomeruli, and this miRNA influences TGF-β -induced collagen 1-α2 expression by downregulating E-box repressors 36. [score:6]
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Reports have shown that several miRNAs (miR-192, −194, −204, −215, and −216) are highly and quite exclusively expressed in the kidney [25], of which miR-192 was found to target SIP1, a major effector of the TGF-β signaling pathway [10]. [score:5]
Increasing evidence, predominantly from animal mo dels of diabetes, shows that several fibrosis-related miRNAs, including miR-192 [10, 11], miR-21 [12], miR-377 [13], and miR-221 [14], are involved in hyperglycemic conditions in different intrinsic renal cell types. [score:1]
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Other miRNAs from this paper: rno-mir-346, rno-mir-146a, rno-mir-146b
Li et al. showed that miR-192 was downregulated in RA synovial tissues [19]. [score:4]
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Further evidence for a coordinate responses in fatty liver disease was obtained by considering regulation of the ER lipid raft associated 2, PPARγ and insulin induced gene 1 by miR-192-5p. [score:4]
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In our study miR-215, part of the miR-192/miR-215 cluster, and miR-34c, involved in DNA damage mediated proliferation arrest [36], [37], [38], [39], were up-regulated, consistent with the pharmacological effect of DOX. [score:4]
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Similarly, Wang et al. [14] found that miR-122a, which is specifically expressed in the liver, was circulating systemically in mice with acetaminophen- (APAP-) induced hepatotoxicity; the authors reported that miR-122a and miR-192 were detected in plasma as early as the point when elevated alanine aminotransferase activity was found evident. [score:3]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Several miRNAs were found to be highly expressed in particular tissues: miR-204, -218, and -129-2-3p in brain tissues, miR-30a, -30e, -30d, -200a and -200b in kidney, miR-192 in liver, miR-451 in spleen, miR-21 in spleen and thymus, miR-193b, -378 in LDM muscle. [score:3]
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In vitro, miR-192 is induced by TGF-β1 and mediates TGF-β–induced collagen expression in mesangial cells [18]. [score:3]
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Specifically, some studies have focused on the roles of miRNAs in the protective effects of fish oil or omega-3 PUFAs against metabolic syndrome and found that the intake of fish oil or DHA/EPA can modify the expression of miR-30b and miR-378 [49], miR-33a and miR-122 [50], miR-107 [51], miR-192, and miR-30c [52]. [score:3]
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Comparison of whey qPCR analyses using the same volumes of samples showed that levels of some miRNAs, such as let-7c, miR-29a, miR-29c, miR-192, miR-21, miR-146a, miR-150, miR-223, and miR-320, did not change during the lactation period (Fig. 6). [score:1]
Comparison of whey and serum qPCR analyses using the same volumes of samples showed that only miR-192, miR-150, and miR-223 (apart from the tissue-specific miRNAs miR-451 and miR-122) were detected at higher levels in serum than in whey. [score:1]
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Interestingly, one miRNA cluster (composed by miR-192 and miR-194a) appears to be regulated by the same lincRNA (lincRNA 555, ENSSSCT00000033052). [score:2]
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A number of miRNAs have been shown to be relevant to fibrotic processes in diabetic nephropathy, including miR-29 and miR-200 families, miR-192 and miR-21 [14– 17]. [score:1]
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Recently Kato et al. showed that miRNA miR-192 has been associated with TGF-β pathway in diabetic kidney glomeruli [78]. [score:1]
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in the brain specimens and sixteen miRNAs (mir-192, mir-148a, mir-122, etc. ) [score:1]
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For example, miR-105, miR-125b and miR-140 are involved in the inflammatory phase; miR-15a, miR-15b and miR-16 participate in the granulation phase; and miR-29 and miR-192 function in the remo deling phase [10]. [score:1]
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