LncRNA PFL contributes to cardiac fibrosis by acting as a competing endogenous RNA of let-7d.

Theranostics
Haihai LiangHongli Shan

Abstract

Rationale: Cardiac fibrosis is associated with various cardiovascular diseases and can eventually lead to heart failure. Dysregulation of long non-coding RNAs (lncRNAs) has recently been recognized as one of the key mechanisms involved in cardiac diseases. However, the potential roles and underlying mechanisms of lncRNAs in cardiac fibrosis have not been explicitly delineated. Methods and Results: Using a combination of in vitro and in vivo studies, we identified a lncRNA NONMMUT022555, which is designated as a pro-fibrotic lncRNA (PFL), and revealed that PFL is up-regulated in the hearts of mice in response to myocardial infarction (MI) as well as in the fibrotic cardiac fibroblasts (CFs). We found that knockdown of PFL by adenoviruses carrying shRNA attenuated cardiac interstitial fibrosis and improved ejection fraction (EF) and fractional shortening (FS) in MI mice. Further study showed that forced expression of PFL promoted proliferation, fibroblast-myofibroblast transition and fibrogenesis in mice CFs by regulating let-7d, whereas silencing PFL mitigated TGF-β1-induced myofibroblast generation and fibrogenesis. More importantly, PFL acted as a competitive endogenous RNA (ceRNA) of let-7d, as forced expression of PFL reduce...Continue Reading

Citations

Jun 29, 2018·American Journal of Physiology. Lung Cellular and Molecular Physiology·Hua JiangHaihai Liang
Apr 24, 2018·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Xuelian LiHaihai Liang
Jan 16, 2019·Cell Death and Differentiation·Yingzhun ChenHaihai Liang
Jun 27, 2019·Journal of Cellular and Molecular Medicine·Wei ZhangXiang Zhou
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