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MiR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE254786 | GEO | 2025/01/30

REPOSITORIES: GEO

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miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [PAR-CLIP]

Project description:In this study, we evaluated genetic mouse models of inducible renal epithelia-specific miR-17~92 loss-of-function and gain-of-function using unilateral ureteral obstruction. We utilized PAR-CLIP in HK2 cells to identify miR-17/-20a targets, which we subsequently validated in vitro. We examined expression of a novel miR-17/-20a target in human nephrectomy samples with varying degrees of fibrosis. We identify an activator of Hippo signaling, FERM domain-containing protein 6 (FRMD6, also known as Willin), as a novel miR-17/20a target. Frmd6 is upregulated in tubular epithelium of obstructed kidneys that lack miR-17~92, along with increased phosphorylation of Smad3 and STAT3, two known miR-17~92 profibrotic targets. Frmd6 overexpression is sufficient to result in elevated secretion of the extracellular matrix component collagen III in vitro. Finally, we demonstrate that FRMD6 expression is associated with collagen III expression in human nephrectomy samples.Our findings demonstrate that the miR-17~92 cluster in renal epithelia functions in an anti-fibrotic manner by regulating multiple pro-fibrotic pathways. We also identify Frmd6 as a novel miR-17/20a target in renal epithelia, which may drive renal fibrosis.

2025-01-30 | GSE254785 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [miRNA-seq]

2025-01-30 | GSE254784 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [RNA-seq]

2025-01-30 | GSE254782 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia

Project description:miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia

| PRJNA1071693 | ENA

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [miRNA-seq]

Project description:miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [miRNA-seq]

| PRJNA1071690 | ENA

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [RNA-seq]

Project description:miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [RNA-seq]

| PRJNA1071691 | ENA

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [PAR-CLIP]

Project description:miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [PAR-CLIP]

| PRJNA1071699 | ENA

Dysregulation of valvular interstitial cell let-7c, miR-17, miR-20a, and miR-30d in naturally occurring canine myxomatous mitral valve disease.

Project description:Canine myxomatous mitral valve disease (MMVD) resembles the early stages of myxomatous pathology seen in human non-syndromic mitral valve prolapse, a common valvular heart disease in the adult human population. Canine MMVD is seen in older subjects, suggesting age-related epigenetic dysregulation leading to derangements in valvular cell populations and matrix synthesis or degradation. We hypothesized that valvular interstitial cells (VICs) undergo disease-relevant changes in miRNA expression. In primary VIC lines from diseased and control valves, miRNA expression was profiled using RT-qPCR and next generation sequencing. VICs from diseased valves showed phenotypic changes consistent with myofibroblastic differentiation (vimentinlow+, α-SMAhigh+), increases in senescence markers (p21, SA-β-gαl), and decreased cell viability and proliferation potential. RT-qPCR and miRNA sequencing analyses both showed significant (p<0.05) downregulation of let-7c, miR-17, miR-20a, and miR-30d in VICs from diseased valves compared to controls. Decreased let-7c, miR-17, and miR-20a may contribute to myofibroblastic differentiation in addition to cell senescence, and decreased miR-30d may disinhibit cell apoptosis. These data support the hypothesis that epigenetic dysregulation plays an important role in age-related canine MMVD.

| S-EPMC5760013 | biostudies-literature

miR-132 mediates renal fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-02-16 | E-GEOD-76550 | biostudies-arrayexpress

miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging.

Project description:Aging is a multifactorial process where deterioration of body functions is driven by stochastic damage while counteracted by distinct genetically encoded repair systems. To better understand the genetic component of aging, many studies have addressed the gene and protein expression profiles of various aging model systems engaging different organisms from yeast to human. The recently identified small non-coding miRNAs are potent post-transcriptional regulators that can modify the expression of up to several hundred target genes per single miRNA, similar to transcription factors. Increasing evidence shows that miRNAs contribute to the regulation of most if not all important physiological processes, including aging. However, so far the contribution of miRNAs to age-related and senescence-related changes in gene expression remains elusive. To address this question, we have selected four replicative cell aging models including endothelial cells, replicated CD8(+) T cells, renal proximal tubular epithelial cells, and skin fibroblasts. Further included were three organismal aging models including foreskin, mesenchymal stem cells, and CD8(+) T cell populations from old and young donors. Using locked nucleic acid-based miRNA microarrays, we identified four commonly regulated miRNAs, miR-17 down-regulated in all seven; miR-19b and miR-20a, down-regulated in six models; and miR-106a down-regulated in five models. Decrease in these miRNAs correlated with increased transcript levels of some established target genes, especially the cdk inhibitor p21/CDKN1A. These results establish miRNAs as novel markers of cell aging in humans.

| S-EPMC2848978 | biostudies-literature

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