Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

• DOI: 10.3892/mmr.2017.7584
• Publication Date: 2017-09-21T08:09:09Z
• Authors: Yuzhen Wei; Xiaofei Yan; Lianhua Yan; Fen Hu; Wenhan Ma; Ya Wang; Shuai Lu; Qiutang Zeng; Zhaohui Wang
• Keywords: Cardiac Fibrosis; Pressure overload; Myocardial fibrosis; Myofibroblast

Cardiac fibrosis triggered by pressure overload represents one of the major challenges in treatment cardiovascular diseases. MicroRNA (miRNA/miR)‑155, a member small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, effect miR‑155 on induced angiotensin II (Ang II), particularly fibroblasts, requires further investigation. The present study aimed investigate Ang II‑induced using animal models and fibroblasts. Animal were established male miR‑155‑/‑ wild‑type (WT) C57Bl/6J mice (10‑12 weeks old) infusion subcutaneously implanted minipumps. After 8 infusion, results that deletion markedly ameliorated ventricular remodeling compared WT mice, as restricted inflammatory responses, decreased heart size, improved function reduced myocardial fibrosis. In vitro, overexpression fibroblasts led significantly increased fibroblast myofibroblast transformation. this was abrogated silencing. conclusion, indicate genetic loss ameliorates fibrotic following overload. Therefore, inhibiting may have potential an adjunct reduce inflammation