Endoplasmic reticulum stress-mediated aldosterone-induced apoptosis in vascular endothelial cells.
10.1007/s11596-014-1359-0
- Author:
Jin-ping LU
1
;
Xia LI
;
Ya-lei JIN
;
Mei-xiang CHEN
Author Information
1. Department of Internal Medicine & Geriatrics, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China, lujp1024@163.com.
- Publication Type:Journal Article
- MeSH:
Aldosterone;
pharmacology;
Apoptosis;
drug effects;
Endoplasmic Reticulum Stress;
drug effects;
Gene Expression Regulation;
drug effects;
Heat-Shock Proteins;
biosynthesis;
Human Umbilical Vein Endothelial Cells;
cytology;
metabolism;
Humans;
Transcription Factor CHOP;
biosynthesis
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(6):821-824
- CountryChina
- Language:English
-
Abstract:
The aim of this study was to examine the effects of endoplasmic reticulum (ER) stress on aldosterone (Aldo)-induced apoptosis of endothelial cells. Glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP, a hallmark of ER-associated apoptosis) were used to evaluate ER stress. Western blotting and real-time PCR were used to analyze indicators of ER molecule. Apoptosis was detected by annexin V/propidium iodide staining and flow cytometry. Human umbilical vein endothelial cells (HUVECs) were stimulated with different concentrations of Aldo for different durations. Aldo promoted apoptosis of HUVECs and induced ER stress, as evidenced by increased expression of GRP78 and CHOP. siRNA knockdown of CHOP attenuated Aldo-mediated apoptosis. These results indicate that ER stress may be involved in Aldo-induced apoptosis of HUVECs.
