Open AccessmiRNA-9 inhibits apoptosis and promotes proliferation in angiotensin II-induced human umbilical vein endothelial cells by targeting MDGA2
Author(s) -
Kai Tan,
Yiping Ge,
Jianhui Tian,
Shaohua Li,
Zhexun Lian
Publication year - 2019
Publication title -
reviews in cardiovascular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.555
H-Index - 39
eISSN - 2153-8174
pISSN - 1530-6550
DOI - 10.31083/j.rcm.2019.02.514
Subject(s) - umbilical vein , apoptosis , angiotensin ii , medicine , microrna , human umbilical vein endothelial cell , cancer research , microbiology and biotechnology , population , endothelial stem cell , renin–angiotensin system , endocrinology , biology , receptor , gene , in vitro , biochemistry , blood pressure , environmental health
Hypertension is a universal risk factor for a variety of cardiovascular diseases. Investigation of the mechanism for hypertension will benefit around 40% of the world's adult population. MicroRNA is crucial for the initiation and progression of cardiovascular diseases. In this study, angiotensin II-treated human umbilical vein endothelial cells were used as a model to imitate the pathological changes in endothelial cells under hypertensive conditions. We demonstrated that microRNA-9 (miR-9) suppressed angiotensin II-induced apoptosis and enhanced proliferation in human umbilical vein endothelial cells. Direct interaction between miR-9 and mitochondria associated membrance domain containing glycosylphosphatidylinositol anchor 2 (MDGA2) was determined. Moreover, miR-9 suppressed MDGA2 levels by binding to the 3' UTR site of the MDGA2 gene. This negative regulation of MDGA2 by miR-9 significantly increased proliferation and decreased apoptosis. Re-introduction of MDGA2 in the miR-9 overexpressed human umbilical vein endothelial cells and normalized proliferation, apoptosis, and the cell cycle. In summary, the present study demonstrated miR-9 inhibited expression of MDGA2 leading to the inhibition of apoptosis and promotion of proliferation in angiotensin II-treated human umbilical vein endothelial cells.