1. MiR-574–5p promotes the differentiation of human cardiac fibroblasts via regulating ARID3A.
- Author
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Cui, Jun, Qi, Siyi, Liao, Rongheng, Su, Diansan, Wang, Yongyi, and Xue, Song
- Subjects
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MYOFIBROBLASTS , *FIBROBLASTS , *HEART fibrosis , *MYOCARDIAL infarction , *FIBROSIS - Abstract
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. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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