MiR-574–5p promotes the differentiation of human cardiac fibroblasts via regulating ARID3A

• Published in: Biochemical and biophysical research communications Vol. 521; no. 2; pp. 427 - 433
• Main Authors: Cui, Jun, Qi, Siyi, Liao, Rongheng, Su, Diansan, Wang, Yongyi, Xue, Song
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 08.01.2020
• Subjects: ARID3A; Cardiac fibrosis; Human cardiac fibroblasts; miR-574–5p; Cardiac fibrosis; ARID3A; miR-574–5p; Human cardiac fibroblasts
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2019.09.107

Cardiac fibrosis after myocardial infarction (MI) is mainly associated with cardiac fibroblasts and its differentiation is the key pathological process. However, the cellular mechanism of fibroblast-to-myofibroblast conversion has not been clarified and a deeper mechanistic understanding is needed. We found that miR-574–5p was up-regulated in TGF-β-induced myofibroblast differentiation. Silencing transiently miR-574–5p in HCFs, we found that suppression of miR-574–5p decreased myofibroblasts differentiation as validated by expression levels of fibrosis related genes, EDU imaging assay, wound healing assay and transwell assays. Conversely, overexpression of miR-574–5p displayed opposite results. ARID3A was verified as a direct target gene of miR-574–5p and decreased level of ARID3A forced fibroblast-to-myofibroblast differentiation of TGF-β-induced HCFs. Our data suggests that miR-574–5p plays a pivotal role in human cardiac fibroblasts (HCFs) myofibroblast differentiation and demonstrates that miR-574–5p and arid3a may be a novel therapeutic target for cardiac fibrosis. •We first demonstrated that miR-574–5p promotes the differentiation of HCFs.•ARID3A is the direct target gene of miR-574–5p.•Suppression of ARID3A recovered the anti-fibrotic response of miR-574–5p knockdown on TGF-β stimulation.