Upregulation of Fas and FasL in Taiwan cobra phospholipase A(2)-treated human neuroblastoma SK-N-SH cells through ROS- and Ca(2+)-mediated p38 MAPK activation.
 

Posts


Write a Post
11-15-08 08:15 AM
Anonymous
Upregulation of Fas and FasL in Taiwan cobra phospholipase A(2)-treated human neuroblastoma SK-N-SH cells through ROS- and Ca(2+)-mediated p38 MAPK activation.
Reply

Upregulation of Fas and FasL in Taiwan cobra phospholipase A(2)-treated human neuroblastoma SK-N-SH cells through ROS- and Ca(2+)-mediated p38 MAPK activation.

J Cell Biochem. 2008 Nov 13;

Authors: Chen KC, Kao PH, Lin SR, Chang LS

The aim of the present study is to elucidate the signaling pathway involved in death of human neuroblastoma SK-N-SH cells induced by Naja naja atra phospholipase A(2) (PLA(2)). Upon exposure to PLA(2), p38 MAPK activation, ERK inactivation, ROS generation, increase in intracellular Ca(2+) concentration, and upregulation of Fas and FasL were found in SK-N-SH cells. SB202190 (p38MAPK inhibitor) suppressed upregulation of Fas and FasL. N-Acetylcysteine (ROS scavenger) and BAPTA-AM (Ca(2+) chelator) abrogated p38 MAPK activation and upregulation of Fas and FasL expression, but restored phosphorylation of ERK. Activated ERK was found to attenuate p38 MAPK-mediated upregulation of Fas and FasL. Deprivation of catalytic activity could not diminish PLA(2)-induced cell death and Fas/FasL upregulation. Moreover, the cytotoxicity of arachidonic acid and lysophosphatidylcholine was not related to the expression of Fas and FasL. Taken together, our results indicate that PLA(2)-induced cell death is, in part, elicited by upregulation of Fas and FasL, which is regulated by Ca(2+)- and ROS-evoked p38 MAPK activation, and suggest that non-catalytic PLA(2) plays a role for the signaling pathway. J. Cell. Biochem. (c) 2008 Wiley-Liss, Inc.

PMID: 19009558 [PubMed - as supplied by publisher]