Severe cell fragmentation in the endothelial cell apoptosis induced by snake apoptosis toxin VAP1 is an apoptotic characteristic controlled by caspases

Toxicon. 2005 Jul;46(1):1-6. doi: 10.1016/j.toxicon.2005.02.002.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Apoptosis Regulatory Proteins
  • Caspase Inhibitors
  • Caspases / metabolism*
  • Cells, Cultured
  • Crotalid Venoms / pharmacology*
  • Endothelial Cells / drug effects*
  • Endothelial Cells / enzymology
  • Endothelial Cells / ultrastructure
  • Humans
  • Metalloendopeptidases / pharmacology*
  • Snake Venoms

Substances

  • Apoptosis Regulatory Proteins
  • Caspase Inhibitors
  • Crotalid Venoms
  • Snake Venoms
  • Caspases
  • Metalloendopeptidases
  • vascular apoptosis-inducing protein 1, Crotalus atrox