[CircRNA_005647 inhibits expressions of fibrosis-related genes in mouse cardiac fibroblasts <i>via</i> sponging miR-27b-3p].

Abstract

OBJECTIVE: To investigate the effect of circRNA_005647 on fibrotic phenotype of mouse cardiac fibroblasts (CFs) and explore its mechanism. METHODS: We used an angiotensin Ⅱ (Ang-Ⅱ) capsule pump (daily dose of 1.46 mg/kg for 2 weeks) to establish a mouse model of myocardial fibrosis in C57BL/6 mice. Masson staining was used to detect myocardial fibrosis in the myocardium. The expression of circRNA_005647 in the myocardium of Ang-Ⅱ-infused mice and in Ang-Ⅱ-treated CFs were detected with real-time PCR. Actinomycin D and RNase R exonuclease digestion were used to test the stability of circRNA_005647 in mouse CFs. Over- expression of circRNA_005647 was achieved in the CFs by infecting the cells with a recombinant circRNA_005647 adenovirus (rAd-circRNA_005647), and the expressions of Col1a1, Col3a1 and Acta2 were detected in the cells with real-time PCR and Western blotting. Dual luciferase reporter assay, RNA antisense purification and RNA Pull down assay were performed to identify the interaction between circRNA_005647 and miR-27b-3p. RESULTS: < 0.05). CONCLUSIONS: CircRNA_005647 is upregulated in cardiac fibrosis and inhibits the expression of fibrosis-related genes through sponging miR-27b-3p in mouse CFs.