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

Ku Chung Chen, Pei Hsiu Kao, Shinne Ren Lin, Long Sen Chang

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

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 A2 (PLA2). Upon exposure to PLA2, 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 PLA2-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 PLA2-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 PLA2 plays a role for the signaling pathway. J. Cell. Biochem. 106: 93-102, 2009.

Original languageEnglish
Pages (from-to)93-102
Number of pages10
JournalJournal of Cellular Biochemistry
Volume106
Issue number1
DOIs
Publication statusPublished - Jan 1 2009
Externally publishedYes

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Elapidae
Phospholipases A
Phospholipases A2
p38 Mitogen-Activated Protein Kinases
Neuroblastoma
Taiwan
Up-Regulation
Chemical activation
Cell death
Cell Death
Lysophosphatidylcholines
Phosphorylation
Acetylcysteine
Cytotoxicity
Chelating Agents
Arachidonic Acid
Catalyst activity

Keywords

  • Ca
  • Fas/FasL upregulation
  • P38 mapk activation
  • Phospholipase A
  • ROS

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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. / Chen, Ku Chung; Kao, Pei Hsiu; Lin, Shinne Ren; Chang, Long Sen.

In: Journal of Cellular Biochemistry, Vol. 106, No. 1, 01.01.2009, p. 93-102.

Research output: Contribution to journalArticle

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abstract = "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 A2 (PLA2). Upon exposure to PLA2, 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 PLA2-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 PLA2-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 PLA2 plays a role for the signaling pathway. J. Cell. Biochem. 106: 93-102, 2009.",
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