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Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts [mRNA]

ABSTRACT: To study and correlate modulations of miRNome with modifications of transcriptome in human stress-induced senescent fibroblasts, Agilent microarrays data were compared by bioinformatics analysis with a focus on ECM components. We identified two unreported direct interactions since we highlighted a reduction in the expression of both miR-22-5p and -199a-5p in senescent fibroblasts, correlated to an increase of MMP1 expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE77074 | GEO | 2022/01/09

REPOSITORIES: GEO

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Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts [miRNA]

Project description:To study and correlate modulations of miRNome with modifications of transcriptome in human stress-induced senescent fibroblasts, Agilent microarrays data were compared by bioinformatics analysis with a focus on ECM components. We identified two unreported direct interactions since we highlighted a reduction in the expression of both miR-22-5p and -199a-5p in senescent fibroblasts, correlated to an increase of MMP1 expression.

2022-01-09 | GSE77406 | GEO

Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts

Project description:Identification of new microRNA-22-5p and -199a-5p/MMP1 functional interactions in stress-induced senescent human dermal fibroblasts

| PRJNA310229 | ENA

MiR-199a-5p determines fibroblast activation and pulmonary fibrogenesis

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal pulmonary disorder characterized by fibroblast proliferation and the excess deposit of extracellular matrix proteins. The etiology of IPF is unknown, but a central role for microRNAs (miRNAs), a class of small non-coding regulatory RNAs, has been recently suggested. We report the upregulation of miR-199a-5p in mouse lungs undergoing bleomycin-induced fibrosis and also in human biopsies from IPF patients. Levels of miR-199a-5p were increased selectively in myofibroblasts and putative profibrotic effects of miR-199a-5p were further investigated in cultured lung fibroblasts. MiR-199a-5p expression was induced upon TGFβ exposure and ectopic expression of miR-199a-5p was sufficient to promote the pathogenic activation of pulmonary fibroblasts. CAV1, a critical mediator of pulmonary fibrosis, was established as a bona fide target of miR-199a-5p. Finally, we also found an aberrant expression of miR-199a-5p in mouse models of kidney and liver fibrosis, suggesting that dysregulation of miR-199a-5p represents a general mechanism contributing to the fibrotic process. We propose miR-199a-5p as a major regulator of fibrosis that represents a potential therapeutic target to treat fibroproliferative diseases. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-02-01 | E-GEOD-34818 | biostudies-arrayexpress

MiR-199a-5p determines fibroblast activation and pulmonary fibrogenesis

2013-02-01 | GSE34818 | GEO

Transcriptome wide target profiling for miR-199a-5p and miR-424-3p.

Project description:Whole transcriptome Identification of direct targets of miR-199a-5p and miR-424-3p using biotinylated pull-downs found that both miRNAs are likely to have a role in the cell cycle. HEK293T cells were transfected with biotinylated miRNAs (either miR-199a-5p or miR-424-3p). The miRNAs and target mRNA were pulled down with streptavidin and compared to the input control.

2013-12-02 | E-GEOD-40406 | biostudies-arrayexpress

Patel2023 - miRNA-199a/b-5p regionation of chondrogenesis - enchanced

Project description:From a previous microarray study we developed a small chondrogenesis model. We performed qPCR and measured how knockdown of miR-199a-5p or miR-199b-5p could modulate chondrogenesis. Several experiments were used to determine the parameters of this model. We utilised parameter scan and manual sliding to refine the model. Within are two models - an initial model which only comprises of genes which we have data for, and an enhanced model which expands of the initial model to make more predictions - e.g. how miR-140-5p is indirectly regulated by miR-199a-5p and miR-199b-5p.

2023-06-06 | MODEL2305010001 | BioModels

Impact of miR-199a-5p silencing on bleomycin-induced lung fibrosis

Project description:To assess the impact of miR-199a-5p silencing on lung fibrogenesis, LNA-miR-199a-5p (5mg/kg) or control formulated for in vivo delivery was instilled intratracheally 4 days and 2 days before intratracheal administration of bleomycin (1 unit/kg) or PBS as well as 4 days after bleomycin or PBS treatment.

2019-04-11 | GSE97825 | GEO

Impact of miR-199-5p, miR-199a-3p and miR-214-3p overexpression on human lung fibroblasts

Project description:To identify putative novel specific targets of miR-199-5p, miR-199a-3p and miR-214-3p, we overexpressed these miRNAs in human MRC5 pulmonary fibroblasts (CCL-171) using synthetic pre-miRNAs or a synthetic “negative” pre-miRNA control (miR-Neg). RNA samples were harvested 48 hours post-transfection and 3 independent experiments were carried out.

2019-04-11 | GSE97824 | GEO

CINC-2 and miR-199a-5p in exosomes secreted by transplanted Thy1+ cells activate hepatocytic progenitor cell growth in rat liver regeneration

Project description:Small hepatocyte-like progenitor cells (SHPCs) are hepatocytic progenitor cells that transiently form clusters in rat livers treated with retrorsine and with 70% partial hepatectomy (PH). We previously reported that transplantation of Thy1+ cells derived from D-galactosamine-treated livers promotes SHPC expansion, resulting in the acceleration of liver regeneration. Extracellular vesicles (EVs) produced by Thy1+ cells act on sinusoidal endothelial cells (SECs) and Kupffer cells to secrete IL17B and IL25, respectively, resulting in SHPC activation through IL17 receptor B (RB) signaling. Our aim is to identify factors in Thy1-EVs that activate IL17RB signaling. Thy1+ cells isolated from rats with D-galactosamine-induced liver injury were cultured for one week. Although some liver stem/progenitor cells proliferated into colonies, others maintained as mesenchymal cells (MCs). Thy1-MCs or Thy1-liver stem/progenitor cells were transplanted into retrorsine/PHtreated livers to examine their effects on SHPCs. SHs isolated from adult rat livers were used to validate factors regulating growth induction. The number and size of SHPCs remarkably increased in livers transplanted with Thy1-MCs. Comprehensive analysis of Thy1-MC-EVs revealed that miR-199a-5p, CINC-2, and MCP-1 are candidates for stimulating SHPC growth. Administration of the miR-199a-5p mimic, and not CINC-2, promoted SH growth. SECs treated with CINC-2 induced IL17b expression and their conditioned medium promoted SH growth. Thy1-MC transplantation may accelerate liver regeneration due to SHPCs expansion, which is stimulated by CINC-2/IL17RB signaling and miR-199a-5p.

2023-04-07 | PXD039384 | Pride

Transcriptome wide target profiling for miR-199a-5p and miR-424-3p.

2013-12-02 | GSE40406 | GEO

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