The molecular mechanism of apoptosis of human umbilical vein endothelial cells induced by monocyte chemotacitic protein-1.
- Author:
Qin-Shan LI
1
;
Yang LIU
;
Zan-Jie FENG
;
Zhi-Shun LU
;
Min-Zhang QIAN
Author Information
1. Department of Biochemistry and Molecular Biology, Zunyi Medical College, Zunyi 563003, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Atherosclerosis;
physiopathology;
Cells, Cultured;
Chemokine CCL2;
metabolism;
Human Umbilical Vein Endothelial Cells;
cytology;
Humans;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
bcl-2-Associated X Protein;
metabolism;
fas Receptor;
metabolism
- From:
Acta Physiologica Sinica
2010;62(1):63-68
- CountryChina
- Language:English
-
Abstract:
The present study was aimed to investigate whether Bcl-2, Fas and Bax are involved in monocyte chemotacitic protein-1 (MCP-1)-induced apoptosis of human umbilical vein endothelial cells (hUVECs). hUVECs were cultured, and the purity was identified by immunofluorescence and immunohistochemistry with specific anti-von Willebrand factor (vWF) and anti-VEGF receptor-2 (KDR) antibodies. With 90% confluence hUVECs were serum-starved for 12 h, and then treated with different concentrations of MCP-1 (0.1, 1.0, 10, 100 ng/mL) for 24 and 48 h respectively. The expressions of apoptosis related proteins Fas, Bcl-2, Bax were detected by flow cytometry (FACS) and Western blot. As shown in our preliminary study, MCP-1 induced apoptosis of hUVECs in a dose-dependent manner at both 24 h and 48 h. FACS and Western blot analysis results in the present study indicated that MCP-1 promoted the expression of proapoptotic proteins Bax and Fas and inhibited the expression of antiapoptotic protein Bcl-2. These results suggest that MCP-1 may induce the apoptosis of hUVECs through evoking the imbalance between proapoptotic Fas/Bax and antiapoptotic Bcl-2 protein.
