Upregulation of Fas and FasL in Taiwan Cobra Phospholipase A2-Treated Human Neuroblastoma SK-N-SH Cells Through ROS- and Ca2+-Mediated p38 MAPK Activation

被引:19
作者
Chen, Ku-Chung [1 ]
Kao, Pei-Hsiu [1 ]
Lin, Shinne-Ren [2 ]
Chang, Long-Sen [1 ]
机构
[1] Natl Sun Yat Sen Univ, Kaohsiung Med Univ, Joint Res Ctr, Inst Biomed Sci, Kaohsiung 804, Taiwan
[2] Kaohsiung Med Univ, Dept Med & Appl Chem, Kaohsiung 807, Taiwan
关键词
PHOSPHOLIPASE A(2); ROS; Ca2+; p38 MAPK ACTIVATION; Fas/FasL UPREGULATION; NADPH OXIDASE; CA2+ INFLUX; A(2); DEATH; EXPRESSION; LIGAND;
D O I
10.1002/jcb.21979
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 Ca2+ 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 (Ca2+ 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 Ca2+-and ROS-evoked p38 MAPK activation, and suggest that non-catalytic PLA(2) plays a role for the signaling pathway. J. Cell. Biochem. 106: 93-102, 2009. (C) 2008 Wiley-Liss, Inc.
引用
收藏
页码:93 / 102
页数:10
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