Abstract:
:This study was designed to elucidate the mechanisms involved in elevated cell death arising from an altered endogenous oxidant state. Increased levels of cell death were detected in cells lacking Gpx1 following the addition of exogenous H2O2. This increased apoptosis correlated with a down-regulation in the activation of the PI(3)K-Akt survival pathway. The importance of this pathway in protecting against H2O2-induced cell death was highlighted by the increased susceptibility of wild-type cells to apoptosis when treated with the PI(3)K inhibitor, LY294002. Activation of the oxidative stress sensitive transcription factor, NFkappaB, was elevated in the Gpx1-/- cells. Significantly, NFkappaB activation could be increased in wild-type cells through the addition of dominant-negative Akt. Therefore, our results suggest that the increased susceptibility of Gpx1-/- cells to H2O2-induced apoptosis can be attributed in part to diminished activation of Akt despite an up-regulation in the activation of the prosurvival NFkappaB. Thus, the PI(3)K-Akt and NFkappaB pathways can act independently of each other in an endogenous model of oxidative stress.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Taylor JM,Crack PJ,Gould JA,Ali U,Hertzog PJ,Iannello RCdoi
10.1016/j.yexcr.2004.07.018keywords:
subject
Has Abstractpub_date
2004-11-01 00:00:00pages
463-75issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(04)00408-2journal_volume
300pub_type
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