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Transforming growth factor-β1 (TGF-β1) plays an important role on fibrogenesis in heart disease. MicroRNAs have exhibited as crucial regulators of cardiac homeostasis and remodeling in various heart diseases.  MiR-19a-3p/19b-3p  expresses with low levels in the plasma of heart failure patients. The purpose of our study is to determine the role of  MiR-19a-3p/19b-3p  in regulating autophagy-mediated fibrosis of human cardiac fibroblasts. We elucidate our hypothesis in clinical samples and human cardiac fibroblasts (HCF) to provide valuable basic information. TGF-β1 promotes collagen I α2 and fibronectin synthesis in HCF and that is paralleled by autophagic activation in these cells. Pharmacological inhibition of autophagy by 3-methyladenine decreases the fibrotic response, while autophagy induction of rapamycin increases the response. BECN1 knockdown and Atg5 over-expression either inhibits or enhances the fibrotic effect of TGF-β1 in experimental HCF. Furthermore,  miR-19a-3p/19b-3p  mimics inhibit epithelial mesenchymal transition (EMT) and extracellular matrix (ECM) prodution and invasion of HCF. Functional studies suggest that  miR-19a-3p/19b-3p  inhibits autophagy of HCF through targeting TGF-β R II mRNA. Moreover, enhancement of autophagy rescues inhibition effect of  miR-19a-3p/19b-3p  on Smad 2 and Akt phosphorylation through TGF-β R II signaling. Our study uncovers a novel mechanism that  miR-19a-3p/19b-3p  inhibits autophagy-mediated fibrogenesis by targeting TGF-β R II.

Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts