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Lipid constituents in oligodendroglial cells alter susceptibility to H 2 O 2 ‐induced apoptotic cell death via ERK activation
Author(s) -
Brand Annette,
Gil Shosh,
Seger Rony,
Yavin Ephraim
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00085.x
Subject(s) - mapk/erk pathway , programmed cell death , microbiology and biotechnology , apoptosis , docosahexaenoic acid , biology , extracellular , oxidative stress , kinase , biochemistry , polyunsaturated fatty acid , fatty acid
The present work examines the effect of membrane lipid composition on activation of extracellular signal‐regulated protein kinases (ERK) and cell death following oxidative stress. When subjected to 50 µ m docosahexaenoic acid (DHA, 22 : 6 n‐3), cellular phospholipids of OLN 93 cells, a clonal line of oligodendroglia origin low in DHA, were enriched with this polyunsaturated fatty acid. In the presence of 1 m m N,N ‐dimethylethanolamine (dEa) a new phospholipid species analog was formed in lieu of phosphatidylcholine. Exposure of DHA‐enriched cells to 0.5 m m H 2 O 2 , caused sustained activation of ERK up to 24 h. At this time massive apoptotic cell death was demonstrated by ladder and TUNEL techniques. H 2 O 2 ‐induced stress applied to dEa or DHA/dEa co‐supplemented cells showed only a transient ERK activation and no cell death after 24 h. Moreover, while ERK was rapidly translocated into the nucleus in DHA‐enriched cells, dEa supplements completely blocked ERK nuclear translocation. This study suggests that H 2 O 2 ‐induced apoptotic cell death is associated with prolonged ERK activation and nuclear translocation in DHA‐enriched OLN 93 cells, while both phenomena are prevented by dEa supplements. Thus, the membrane lipid composition ultimately modulates ERK activation and translocation and therefore can promote or prevent apoptotic cell death.