Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death.

Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Research Abstract Details 

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Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Abstract Text:

Jong-Ok Pyo,Jihoon Nah,Hyo-Jin Kim,Ho-June Lee,Jungun Heo,Heuiran Lee,Yong-Keun Jung,

Despite of the increasing evidence that oxidative stress may induce non-apoptotic cell death or autophagic cell death, the mechanism of this process is unclear. Here, we report a role and a down-stream molecular event of Atg5 during oxidative stress-induced cell death. Compared to wild type (WT) cells, Atg5-deficient mouse embryo fibroblasts (Atg5(-/-) MEFs) and Atg5 knockdown HT22 neuronal cells were more resistant to cell death induced by H(2)O(2). On the contrary, Atg5(-/-) MEFs were as sensitive to tumor necrosis factor (TNF)-alpha and cycloheximide as WT cells, and were more sensitive to cell death triggered by amino acid-deprivation than WT MEFs. Treatment with H(2)O(2) induced the recruitment of a GFP-LC3 fusion protein and conversion of LC3 I to LC3 II, correlated with the extent of autophagosome formation in WT cells, but much less in Atg5-deficient cells. Among stress kinases, ERK1/2 was markedly activated in Atg5(-/-) MEFs and Atg5 knockdown HT22 and SH-SY5Y neuronal cells. The inhibition of ERK1/2 by MEK1 inhibitor (PD98059) or dominant negative ERK2 enhanced the susceptibility of Atg5(-/-) MEFs to H(2)O(2)-induced cell death. Further, reconstitution of Atg5 sensitized Atg5(-/-) MEFs to H(2)O(2) and suppressed the activation of ERK1/2. These results suggest that the inhibitory effect of Atg5 deficiency on cell death is attributable by the compensatory activation of ERK1/2 in Atg5(-/-) MEFs during oxidative stress-induced cell death.

Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Publishing Authors By Initials

JO Pyo,J Nah,HJ Kim,HJ Lee,J Heo,H Lee,YK Jung,

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Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Autophagy

VOLUME: 4

Page Numbers: 315-21

Journal Abbreviation: Autophagy

ISSN: 1554-8635

DAY: 7

MONTH: 01

YEAR: 2008

Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death.

AFFILIATION: School of Biological Science/Bio-MAX Institute, Seoul National University, Shillim-dong, Gwanak-gu, Seoul, Korea.

Country: United States

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MEDLINETA: Autophagy

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