Zhao Qitao, Araki Satohiko, Zhang ShangLi, Miao Junying
Department of Biology, Institute of Developmental Biology, School of Life Science, Shandong University, No. 27 Southern Shanda Road, Jinan 250100, China.
Toxicon. 2004 Aug;44(2):161-8. doi: 10.1016/j.toxicon.2004.05.015.
In the previous studies, we found that phosphatidylcholine-specific phospholipase C (PC-PLC) was implicated in apoptosis induced by rattlesnake venom in vascular endothelial cells (VEC) [Biochem. Biophys. Res. Commun. (1997b) 223, 182]. In order to find out other signal elements in this pathway and the mechanisms by which PC-PLC mediates apoptosis induced by rattlesnake venom in VEC, the expression of integrin beta4 and P53 was evaluated when the activity of PC-PLC was suppressed by D609 (tricyclodecan-9-yl-xanthogenate), a specific inhibitor of this enzyme. The increase of integrin beta4 and P53 expression induced by the venom was markedly suppressed when apoptosis of VEC was inhibited by D609. The data indicated that integrin beta4 and P53 play important roles in signal transduction of apoptosis induced by rattlesnake venom, and that PC-PLC might regulate apoptosis by up-regulating the expression of integrin beta4 and P53 in VEC.
在先前的研究中，我们发现磷脂酰胆碱特异性磷脂酶C（PC-PLC）与响尾蛇毒液诱导血管内皮细胞（VEC）凋亡有关[《生物化学与生物物理研究通讯》（1997b年）第223卷，第182页]。为了找出该途径中的其他信号元件以及PC-PLC介导响尾蛇毒液诱导VEC凋亡的机制，当PC-PLC的活性被该酶的特异性抑制剂D609（三环癸烷-9-基-黄原酸酯）抑制时，对整合素β4和P53的表达进行了评估。当D609抑制VEC凋亡时，毒液诱导的整合素β4和P53表达增加受到明显抑制。数据表明，整合素β4和P53在响尾蛇毒液诱导的凋亡信号转导中起重要作用，并且PC-PLC可能通过上调VEC中整合素β4和P53的表达来调节凋亡。
