Role of miR-24 in myocardial fibrosis induced by angiotensin II

Objective: To investigate the role and mechanism of miR-24 in angiotensin II induced myocardial fibrosis, by miR-24 expression and interference recombinant lentiviral transduction in primary cardiac fibroblasts. Method: The primary cardiac fibroblasts were stimulated by angiotensin II to simulate in vitro myocardial fibrosis. Cardiac fibroblasts were transduced with previously constructed miR-24 expression interference recombinant lentivirus. Cell proliferation, apoptosis and gene expression levels of AGTR-1, ß-arrestin-1, GNAQ and PKC-delta were detected to identify the target of miR-24. PKC-delta expression recombinant lentivirus was constructed to investigate the effect of miR-24 on AGTR1-Gq-PKC signaling pathway. Results: MiR-24 facilitated expression of AGTR-1 and ß-arrestin-1 and cell apoptosis, and inhibited cell proliferation and the synthesis of hydroxyproline, exhibiting a negative synergistic effect with PKC-delta. Conclusion: miR-24 negatively regulated PKC-delta by working on AGTR1 and furthermore inhibited myocardial fibrosis induced by angiotensin II.