Open AccessEffects of Pitavastatin on the Expression of VCAM ‐1 and its Target Gene miR‐126 in Cultured Human Umbilical Vein Endothelial Cells
Author(s) -
Xu Qinglu,
Luan Tianzhu,
Fu Songbin,
Yang Jian,
Jiang Chao,
Xia Fangfang
Publication year - 2014
Publication title -
cardiovascular therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 46
eISSN - 1755-5922
pISSN - 1755-5914
DOI - 10.1111/1755-5922.12081
Subject(s) - pitavastatin , umbilical vein , vcam 1 , cell adhesion molecule , medicine , human umbilical vein endothelial cell , messenger rna , blot , tumor necrosis factor alpha , inflammation , endothelial stem cell , proinflammatory cytokine , endocrinology , statin , microbiology and biotechnology , pharmacology , icam 1 , immunology , biology , in vitro , gene , biochemistry
Summary Objectives Reducing the expression of endothelial cell adhesion molecules is conducive to the decrease of inflammation‐induced vascular complications. In this study, we observed pitavastatin on expression of vascular cell adhesion molecule‐1 ( VCAM ‐1) and its influence on VCAM ‐1's target gene miR‐126 in endothelial cells. The purpose of this study is to explore the mechanism of pitavastatin in prevention and treatment of atherosclerosis. Methods HUVEC were cultured in M1640 and passages 2–5 were used in experiments. The cells were randomly divided into three groups, control, TNF‐ α and pitavastatin group. Cells of TNF‐ α group were co‐incubated with different concentrations (10, 20, 30 μ g/L) of TNF‐ α for 24 h. Cells of pitavastatin group were firstly coincubated with (0.01, 0.1, 1 μ mol/L) pitavastatin, respectively, for 1 h, then coincubated with 30 μ g/L TNF‐ α for 24 h. VCAM‐1 and miR‐126 mRNA were detected by RT‐PCR, and Western blotting was used to detect protein expression of VCAM‐1. Results Both detection methods have showed that TNF‐ α stimulation significantly increased the mRNA and protein expression of VCAM‐1 in a dose‐dependent manner, and miR‐126 mRNA expression exhibited a decreasing trend. The increase of VCAM‐1 mRNA and protein expression induced by TNF‐ α was inhibited by pitavastatin in a dose‐dependent manner, too. However, there were no differences of the expression of miR‐126 among three groups. Conclusions These effects may explain the ability of pitavastatin to reduce the progression of atherosclerosis. The findings further suggest that inhibitory effect of pitavastatin on VCAM ‐1 is not related to miR‐126 but depends on other ways.