Panminerva Medica 2020 Jul 27

DOI: 10.23736/S0031-0808.20.03975-0

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

MiR-29c-3p inhibits proliferation and migration in rat primary cardiac fibroblasts via interacting with STAT3

Sha YE ¹, Cuiling YANG ¹, Chunya WANG ², Aiping JIN ¹, Qianrong ZHANG ¹, Suilong ZHANG ¹ ✉

¹ Department of Geriatric Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China; ² Department of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China

BACKGROUND: To elucidate the influence and molecular mechanism of microRNA-29c-3p (miR-29c-3p) on cell functions of cardiac fibroblasts.
METHODS: Rat primary cardiac fibroblasts were induced with high-level glucose (HG), followed by determination of miR-29c-3p and signal transducer and activator of transcription 3 (STAT3) levels. The regulatory effects of miR-29c-3p and STAT3 (AG490) on proliferative and migratory potentials in HG-induced cardiac fibroblasts were examined by cell counting kit-8 (CCK-8) and transwell assay, respectively. The interaction between miR-29c-3p and STAT3 was assessed by bioinformatics analysis and dual-luciferase reporter assay.
RESULTS: MiR-29c-3p was downregulated, and STAT3 was upregulated in HG-induced cardiac fibroblasts. HG induction stimulated proliferative and migratory potentials in cardiac fibroblasts, which were attenuated by overexpression of miR-29c-3p. STAT3 was the target gene binding miR-29c-3p. Application of AG490, the STAT3 inhibitor, was able to reverse the promoted proliferative and migratory potentials in HG-induced cardiac fibroblasts with miR-29c-3p knockdown.
CONCLUSIONS: MiR-29c-3p weakens the over-proliferative and over-migratory potentials in HG-induced cardiac fibroblasts via inactivating the STAT3 signaling.

KEY WORDS: MiR-29c-3p; STAT3; Diabetic cardiomyopathy; Cardiac fibroblasts