Clonidine induces rat aorta relaxation by nitric oxide-dependent and -independent mechanisms

To find more effective components which can trigger apoptosis in crude rattlesnake venom, and the possible mechanisms by which the venom causes apoptosis in vascular endothelial cells (VECs), we investigated the function of integrin beta4 by using the monoclonal antibody (mAb) of this integrin. We added anti-beta4 mAb 5 microg.ml(-1) to the cells treated with 2 microg.ml(-1) rattlesnake venom; apoptosis of these cells was completely inhibited 6 h after the treatment. Furthermore, the increase of P53 expression induced by the venom was markedly suppressed. The results first demonstrated that there was at least one important component target to integrin beta4 in crude rattlesnake (Crotalus atrox) venom; moreover, this component played its role in the early phase of apoptosis. The results also showed that integrin beta4 participated in signal transduction of apoptosis induced by rattlesnake venom in VEC by up-regulating the expression of p53.