JNK1/c-Jun and p38α MAPK/ATF-2 pathways are responsible for upregulation of Fas/FasL in human chronic myeloid leukemia K562 cells upon exposure to Taiwan cobra phospholipase A2

Ku Chung Chen, Yi Ling Chiou, Long Sen Chang

研究成果: 雜誌貢獻文章

11 引文 斯高帕斯(Scopus)

摘要

Fas and FasL expression upregulation was found in human leukemia K562 cells upon exposure to Naja naja atra phospholipase A2 (PLA2). PLA2 treatment induced an increase in intracellular Ca2+ ([Ca2+]i) and ROS generation levels, leading to activation of p38 MAPK and JNK. Suppression of both p38 MAPK and JNK abrogated Fas and FasL upregulation. Unlike PLA2, catalytically inactive PLA2 treatment did not markedly increase Fas and FasL protein expression, and p38 MAPK activation was exclusively responsible for catalytically inactive PLA 2-induced increase in Fas and FasL protein expression. Knockdown of p38α MAPK and JNK1 by siRNA proved that p38α MAPK and JNK1 were involved in ATF-2 and c-Jun phosphorylation, respectively. Compared with the p38α MAPK/ATF-2 pathway, the JNK1/c-Jun pathway played a crucial role in Fas/FasL upregulation. Unlike arachidonic acid, lysophosphatidylcholine mimicked the PLA2 action in inducing Fas/FasL upregulation. Together with the previous finding that c-Jun and ATF-2 are involved in transcriptional regulation of Fas and FasL, our data suggest that PLA2 induces Fas and FasL upregulation through p38a MAPK/ATF-2 and JNK1/c-Jun pathways in K562 cells, and PLA2 catalytic activity is involved in this action.

原文英語
頁(從 - 到)612-620
頁數9
期刊Journal of Cellular Biochemistry
108
發行號3
DOIs
出版狀態已發佈 - 十月 15 2009
對外發佈Yes

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

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