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MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor ?.

ABSTRACT: Hypertrophic scar (HS) is a dermal fibro-proliferative disorder result from abnormal wound healing after skin injury. MicroRNA-9-5p (miR-9-5p) has been reported to be upregulated and closely related to collagen proteins in human dermal fibroblasts. However, the correlation and possible mechanism between miR-9-5p and HS require further investigation. The expressions of miR-9-5p in HS tissues and HS fibroblasts were detected by quantitative real-time PCR (RT-qPCR). The expression level of peroxisome proliferator-activated receptor ? (PPAR?) was measured by RT-qPCR assay. The protein levels of PPAR?, ?-SMA, Vimentin, COL1A, cyclin D1, bcl-2, and bax were detected by western blot assay. The effect of miR-9-5p and PPAR? on HS fibroblasts proliferation and apoptosis were detected by cell counting kit-8 (CCK-8) and flow cytometry assays. The interaction between miR-9-5p and PPAR? was predicted by TargetScan, and then confirmed by dual-luciferase reporter assay. MiR-9-5p expression was downregulated in HS tissues and HS fibroblasts. MiR-9-5p inhibited the levels of extracellular matrix-associated genes (?-SMA, Vimentin, COL1A) in HS fibroblasts. MiR-9-5p repressed proliferation and induced apoptosis of HS fibroblasts. PPAR? is a target gene of miR-9-5p. The silencing of PPAR? expression hindered proliferation and expedited apoptosis of HS fibroblasts. MiR-9-5p suppressed proliferation and promoted apoptosis of HS fibroblasts by targeting PPAR?. In this paper, we firstly disclosed that miR-9-5p hampered extracellular matrix deposition and proliferation, and induced apoptosis by targeting PPAR? in HS fibroblasts. Our findings provided a new role of miR-9-5p/PPAR? in the occurrence and development of HS fibroblasts, promising a new target for HS.

SUBMITTER: Chai CY

PROVIDER: S-EPMC7774882 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor β.

Chai Chi-Yung CY Tai I-Chun IC Zhou Rui R Song Junlong J Zhang Chaoying C Sun Shengrong S

Biology open 20201221 12

Hypertrophic scar (HS) is a dermal fibro-proliferative disorder result from abnormal wound healing after skin injury. MicroRNA-9-5p (miR-9-5p) has been reported to be upregulated and closely related to collagen proteins in human dermal fibroblasts. However, the correlation and possible mechanism between miR-9-5p and HS require further investigation. The expressions of miR-9-5p in HS tissues and HS fibroblasts were detected by quantitative real-time PCR (RT-qPCR). The expression level of peroxiso ...[more]

PMID: 33355167

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Project description:Peroxisome proliferator-activated receptor γ (PPARγ) has 2 protein isoforms (PPARγ1 and PPARγ2) generated by alternative promoter usage and alternative splicing. However, their functional uniqueness and similarity remain unclear. In the study, we investigated the effects of lentivirus-mediated overexpression of PPARγ1 and PPARγ2 on proliferation, apoptosis, and differentiation of the immortalized chicken preadipocytes. Cell Counting Kit-8 assay showed PPARγ1 and PPARγ2 overexpression markedly suppressed cell proliferation, and fluorescence activated cell sorting analysis showed that PPARγ1 and PPARγ2 overexpression caused cell cycle arrest at G0/G1 phase. Cell death detection ELISA analysis showed both PPARγ1 and PPARγ2 overexpression induced cell apoptosis. Oil red O staining and gene expression analysis showed both PPARγ1 and PPARγ2 overexpression promoted preadipocyte differentiation. In the presence of PPARγ ligand, rosiglitazone, PPARγ2 overexpression was more potent in inducing apoptosis, promoting adipogenesis, and suppressing cell proliferation than PPARγ1 overexpression. We further explored the molecular basis for their functional differences. Reporter gene assay showed that under ligand conditions, PPARγ2 overexpression resulted in 1.68-fold increase in transcription activity compared with PPARγ1. Electrophoretic mobility shift assay showed both PPARγ1 and PPARγ2 could bind to PPAR response element (PPRE) as heterodimer with retinoid X receptor alpha, and by comparison, PPARγ2 had a higher affinity for PPRE than PPARγ1. Reporter gene assay showed expression PPARγ1 and PPARγ2 similarly induced fatty acid synthase and adipocyte fatty acid-binding protein promoter activity but differentially induced lipoprotein lipase and perilipin 1 promoter activities. Coimmunoprecipitation analysis showed that PPARγ1 and PPARγ2 interacted similarly with the coactivators, Tat-interacting protein 60. Taken together, our results demonstrate that PPARγ1 and PPARγ2 differentially regulate preadipocyte proliferation, apoptosis, and differentiation as a result of their distinct and overlapping molecular functions.

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MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor ?.

Publications

MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor β.

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