MicroRNA-199a regulates myocardial fibrosis in rats by targeting SFRP5

M.-H. Chen, J.-C. Liu, Y. Liu, Y.-C. Hu, X.-F. Cai, D.-C. Yin

Department of Emergency Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China. cmh6186@126.com

---

• Cardiology

OBJECTIVE: Myocardial fibrosis seriously affects normal heart function. This study focused on the role of microRNA-199a in regulating rat myocardial fibrosis by targeting secreted frizzled-related protein 5 (SFRP5).
MATERIALS AND METHODS: The in vitro myocardial fibrosis model was established by 10 μM isoproterenol (ISO) induction in cardiac fibroblasts (CFs) for 24 h. Expression levels of microRNA-199a, collagen I and α smooth muscle actin (α-SMA) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein levels of SFRP5 and transforming growth factor-β1 (TGF-β1) in CFs were detected by Western blot. The binding condition between microRNA-199a and SFRP5 was verified by luciferase reporter gene assay. After transfection of microRNA-199a inhibitor or SFRP5 overexpression plasmid, proliferative and migratory rates of CFs were determined by cell counting kit-8 (CCK-8) and transwell assay, respectively.
RESULTS: ISO treatment remarkably upregulated microRNA-199a expression in CFs. Transfection of microRNA-199a inhibitor could inhibit proliferation, migration and cardiac fibroblast-to-myofibroblast transformation (CMT) of CFs. Luciferase reporter gene assay confirmed the binding of microRNA-199a to SFRP5 3’UTR. Moreover, SFRP5 overexpression reversed the effects of microRNA-199a inhibitor on proliferation, migration, and CMT of CFs.
CONCLUSIONS: MicroRNA-199a deficiency can inhibit the proliferative and migratory potentials of CFs, as well as CMT by targeting SFRP5, thus exerting the protective effect on myocardial fibrosis.

This article has been retracted. The Publisher apologizes for any inconvenience this may cause. Retraction note in: Eur Rev Med Pharmacol Sci 2024; 28 (7): 2631-2631.

Free PDF Download