Expressions of p-c-jun and cyclinD1 between vascular smooth muscle cells and endothelial cells exposured to cigarette smoke extract.
- Author:
Tian-jia LI
1
;
Chang-wei LIU
;
Ze-bin HUANG
;
Leng NI
;
Zhi-chao LAI
;
Li-fei WU
;
Bao LIU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Proliferation; drug effects; Cell Survival; Cells, Cultured; Cyclin D1; metabolism; Endothelial Cells; drug effects; metabolism; Humans; Myocytes, Smooth Muscle; drug effects; metabolism; Proto-Oncogene Proteins c-jun; metabolism; Tobacco; adverse effects
- From: Acta Academiae Medicinae Sinicae 2013;35(2):185-189
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the cell viabilities of vascular smooth muscle cells and vascular endothelial cells stimulated by cigarette smoke extract(CSE) .
METHODSThe CSE was prepared by smoke-bubbled phosphate buffered saline(PBS) generation.After culturing cells with different concentrations of CSE, we used the cell counting kit-8 to determine the cell viability.The expression levels of c-jun and cyclinD1 were analyzed through Western blot.The c-jun plasmid was transfected to detect the change of cyclinD1 expression.
RESULTSThe smooth muscle cell viability increased when the CSE concentration ranged 0.625%-10%, whereas the endothelial cells viability decreased when exposed to the CSE concentration. After exposure to CSE for 48 hours, there was no difference in c-jun expression between toxin group and PBS group;however, the expression of p-c-jun in the smooth muscle cells significantly increased in the toxin groups than in the PBS group(P<0.05) and the expression of p-c-jun in the vascular endothelial cells significantly decreased(P<0.05) . The level of cyclinD1 significantly increased after exposed to CSE, and its expression level also increased in respond to the c-jun overexpression.
CONCLUSIONCSE can enhance the proliferation of vascular smooth muscle cells and decrease in the activity of endothelial cells proliferation, which may be explained by the phosphorylation of c-jun and the expression of cyclinD1.