Progress of studies on VEC apoptosis-inducing proteins in snake venom and its mechanism--review.
- Author:
Qi-Tao ZHAO
1
;
Kun XIE
;
Jie ZHANG
;
Jun-Ying MIAO
Author Information
1. Institute of Developmental Biology, School of Life Science, Shandong University, Jinan 250100, China.
- Publication Type:Journal Article
- MeSH:
Amino Acid Oxidoreductases;
pharmacology;
Animals;
Apoptosis;
drug effects;
Endothelial Cells;
cytology;
drug effects;
Gene Expression Regulation;
drug effects;
Humans;
L-Amino Acid Oxidase;
Reactive Oxygen Species;
Signal Transduction;
Snake Venoms;
chemistry;
pharmacology
- From:
Journal of Experimental Hematology
2004;12(5):708-712
- CountryChina
- Language:Chinese
-
Abstract:
Hemorrhagic snake venom specially induces apoptosis of VEC (vascular endothelial cells). Five apoptosis-inducing proteins had been purified and characterized from crude snake venom. Two of these are L-amino acid oxidase (LAO), the others belong to metalloprotease/disintegrin family. LAO catalyzes H2O2 production by oxidizing some plasma membrane proteins of VEC, disintegrins interfere with binding of integrins with their ligands. The expression of p53 and bcl-2 increases during VEC apoptosis induced by snake venom, moreover, the mRNA of bcl-2 is spliced into two fragments. It has been proved that one of adhesion-dependent signal molecules, alphavbeta3, and one of phospholipid signal molecules, PC-PLC (phosphatidylcholine-specific phospholipase C), are involved in above apoptosis-inducing signal transudation pathway. These results throw light on finding out specific component from protein is snake venom. This component is able to induce tumor vascular endothelial cells apoptosis. This review summarized progress of research on hemorrhagic snake venoms.
