MiR-30b-5p and miR-22-3p restrain the fibrogenesis of post-myocardial infarction in mice via targeting PTAFR.

Cardiac fibrosis of post-myocardial infarction (MI) is a precipitating factor of diverse cardiac diseases. MicroRNAs (miRNAs) have been reported to be implicated in the progression of cardiac fibrosis, but the functions and mechanisms of miR-30b-5p and miR-22-3p remain to be investigated. Cardiac fibroblasts (CFs) were isolated form mice hearts and treated with Angiotensin II (Ang II) for establishing the cardiac fibrosis model of post-MI. The expression of miRNA and mRNA was examined through quantitative real-time polymerase chain reaction (qRT-PCR). Associated protein levels were measured by Western blot. Cell viability was detected via cell counting kit-8 (CCK-8) assay. Dual-Luciferase reporter assay was administered to analyze the target correlation. The down-regulation of miR-30b-5p and miR-22-3p while the up-regulation of platelet activating factor receptor (PTAFR) were found in Ang II-treated CFs. Cell proliferation and collagen deposition were refrained by miR-30b-5p and miR-22-3p overexpression and knockdown of PTAFR. MiR-30b-5p and miR-22-3p directly targeted PTAFR. MiR-30b-5p and miR-22-3p inhibitors alleviated the effects on Ang II-treated CFs induced by PTAFR knockdown through promoting PTAFR. MiR-30b-5p and miR-22-3p exerted the suppression of fibrogenesis in Ang II-treated CFs via targeting PTAFR, insinuating the indicative roles of miR-30b-5p and miR-22-3p in the fibrogenesis process.