Premium
Preliminary study on the mechanism of long noncoding RNA SENCR regulating the proliferation and migration of vascular smooth muscle cells
Author(s) -
Ye Famin,
Zhang Jing,
Zhang Qiaoling,
Zhang Jingjing,
Chen Cheng
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29775
Subject(s) - vascular smooth muscle , gene knockdown , microbiology and biotechnology , cell growth , cell migration , biology , cell , cell cycle , untranslated region , messenger rna , cell culture , endocrinology , smooth muscle , gene , genetics
The proliferation and migration of vascular smooth muscle cells (VSMCs) are one of the key regulatory links of atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are emerging as key regulators in AS development. In this study, we first assessed the expression level of smooth muscle and endothelial cell‐enriched migration/differentiation‐associated lncRNA (SENCR) in the plasma of patients with coronary heart disease (CHD) and its predictive and diagnostic value. Second, we investigated the role of SENCR in the regulation network of human aortic‐VSMCs (HA‐VSMCs) proliferation and migration and determined its downstream regulatory mechanism. The results showed that SENCR was downregulated in the peripheral blood of CHD, and negatively related to the Gensini score. SENCR was enriched in HA‐VSMCs and mainly distributed in cytoplasm. Overexpression of SENCR significantly inhibited HA‐VSMCs proliferation, migration, and block cell cycle, while the knockdown of SENCR had the opposite effects. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that miR‐4731‐5p could directly bind to SENCR. Besides, we proved that FOXO3a inhibited HA‐VSMCs proliferation and migration by binding to the 3′‐untranslated region of miR‐4731‐5p. In summary, our research suggested that SENCR affects HA‐VSMCs proliferation and migration via regulating the miR‐4731‐5p/FOXO3a pathway.