UV light induces premature senescence in Akt1-null mouse embryonic fibroblasts by increasing intracellular levels of ROS.

Abstract:

:Akt/PKB plays a pivotal role in cell survival and proliferation. Previously, we reported that UV-irradiation induces extensive cell death in Akt2(-/-) mouse embryonic fibroblasts (MEFs) while Akt1(-/-) MEFs show cell cycle arrest. Here, we find that Akt1(-/-) MEFs exhibit phenotypic changes characteristics of senescence upon UV-irradiation. An enlarged and flattened morphology, a reduced cell proliferation and an increased senescence-associated beta-galactosidase (SA beta-gal) staining indicate that Akt1(-/-) MEFs undergo premature senescence after UV-irradiation. Restoring Akt1 expression in Akt1(-/-) MEFs suppressed SA beta-gal activity, indicating that UV-induced senescence is due to the absence of Akt1 function. Notably, levels of ROS were rapidly increased upon UV-irradiation and the ROS scavenger NAC inhibits UV-induced senescence of Akt1(-/-) MEFs, suggesting that UV light induces premature senescence in Akt1(-/-) MEFs by modulating intracellular levels of ROS. In conjunction with our previous work, this indicates that different isoforms of Akt have distinct function in response to UV-irradiation.

authors

Jee HJ,Kim HJ,Kim AJ,Bae YS,Bae SS,Yun J

doi

10.1016/j.bbrc.2009.04.017

subject

Has Abstract

pub_date

2009-06-05 00:00:00

pages

358-62

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)00698-6

journal_volume

383

pub_type

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