Maruyama Jiro, Hayashi Hiroshi, Miao Junying, Sawada Hitoshi, Araki Satohiko
Sugashima Marine Biological Laboratory, School of Science, Nagoya University, Toba, Mie 517-0004, Japan.
Toxicon. 2005 Jul;46(1):1-6. doi: 10.1016/j.toxicon.2005.02.002.
Hemorrhagic snake venom induces apoptosis in vascular endothelial cells (VEC). Vascular apoptosis-inducing protein 1 (VAP1), which is identified as an apoptosis toxin against vascular endothelial cells, induces apoptosis accompanied by severe cell fragmentation compared with that of apoptosis due to other inducers. The mechanism of this morphologic feature is not known. In this report, we examine the roles of the caspases in the apoptosis induced by VAP1. Measurement of the caspase activities shows that activation of caspases occurred in this type of cell death. In the presence of certain caspase inhibitors, the severe cell fragmentation was strongly inhibited. The other hand, cell death induced by VAP1 was not affected by caspase inhibitors. These data suggest that the severe cell fragmentation induced by the snake toxin is a special characteristic of this apoptosis. Apoptosis with severe cell fragmentation may be regarded as a new category of endothelial cell apoptosis.
出血性蛇毒可诱导血管内皮细胞（VEC）凋亡。血管凋亡诱导蛋白1（VAP1）被鉴定为一种针对血管内皮细胞的凋亡毒素，与其他诱导剂诱导的凋亡相比，它诱导的凋亡伴有严重的细胞碎片化。这种形态学特征的机制尚不清楚。在本报告中，我们研究了半胱天冬酶在VAP1诱导的凋亡中的作用。半胱天冬酶活性的测定表明，在这种类型的细胞死亡中发生了半胱天冬酶的激活。在存在某些半胱天冬酶抑制剂的情况下，严重的细胞碎片化受到强烈抑制。另一方面，VAP1诱导的细胞死亡不受半胱天冬酶抑制剂的影响。这些数据表明，蛇毒诱导的严重细胞碎片化是这种凋亡的一个特殊特征。伴有严重细胞碎片化的凋亡可能被视为一种新的内皮细胞凋亡类型。
