MiR-411-5p Alleviates Angiotensin II-Induced Fibrosis in H9c2 Cells by Inhibiting HCN1

Myocardial fibrosis (MF) is closely related to various cardiovascular diseases, especially heart failure. However, the mechanisms related to the treatment of MF are not entirely clear. Therefore, this study investigated the effects of miR-411-5p and HCN1 on MF alleviation.RT-qPCR and Western blotting were used to determine Ang II-induced fibrosis of H9c2 cells and alterations in miR-411-5p and HCN1 expression. CCK-8, EdU staining, Transwell assay, immunofluorescence staining, and Western blot were used to determine the effects of the corresponding transfectants on H9c2 cell viability, cell proliferation, migration, and fibrosis. Meanwhile, the dual-luciferase report, RNA binding protein immunoprecipitation assay, RT-qPCR, and Western blot were collectively employed to investigate the targetability between miR-411-5p and HCN1.In this study, the optimal concentration of Ang II used to establish fibrosis of H9c2 cells was 10 ng/mL, under which the expression level of miR-411-5p was downregulated but the expression level of HCN1 was upregulated. Enhanced miR-411-5p or HCN1 silencing downregulated the elevation of cell viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs caused by Ang II. MiR-411-5p inhibitors reversed the decline in the viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs induced by sh-HCN1 transfection. In addition, miR-411-5p targets and negatively regulates HCN1 expression.In conclusion, miR-411-5p alleviated Ang II-induced fibrosis of H9c2 cells and primary CFs by inhibiting HCN1.