Anti-apoptosis effect of VEGF on the human chronic myelocytic leukemia cell line K562.
- Author:
Yue-Yong ZHU
1
;
De-Fu YE
;
Jing-An LIN
;
Sheng-Mei WENG
;
Xiao-Hua LIANG
Author Information
1. Department of Hematology, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China. ezhu066@sina.com
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Arsenicals;
pharmacology;
Blotting, Western;
Chlorides;
pharmacology;
Flow Cytometry;
Humans;
K562 Cells;
RNA, Messenger;
genetics;
metabolism;
Reverse Transcriptase Polymerase Chain Reaction;
Vascular Endothelial Growth Factor A;
pharmacology;
bcl-2-Associated X Protein;
biosynthesis;
genetics;
bcl-X Protein;
biosynthesis;
genetics
- From:
Journal of Experimental Hematology
2005;13(5):778-782
- CountryChina
- Language:Chinese
-
Abstract:
To explore the effects of vascular endothelial growth factor (VEGF) on the mechanisms of CML pathogenesis, the effect of VEGF on K562 cell apoptosis induced by As(2)O(3) was analyzed through morphologic observation, DNA fragmentation agarose gel electrophoresis and DNA ploidy flow cytometry analysis, and the effect of VEGF on the expression of bcl-X(L), Bax and caspase-3 in K562 cells was determined by Western blot, meanwhile the expression difference between bcl-X(L) and Bax mRNA in above conditions was detected by RT-PCR. The results showed that after VEGF added, the apoptosis of K562 cells reduced, however, there was no significant changes in cell cycle distribution (P > 0.05). At the same time, following the increasing of the concentration of VEGF, expression of mRNA and protein of bcl-X(L) was up-regulated and the expression of Bax protein was down-regulated in K562 cells, and the activation of pro-caspase-3 into caspase-3 was inhibited or reduced. It is concluded that VEGF may suppress the apoptosis of K562 cells through its influence on the bcl-X(L)/Bax expression ratio in K562 cells.
