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.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Jee HJ,Kim HJ,Kim AJ,Bae YS,Bae SS,Yun Jdoi
10.1016/j.bbrc.2009.04.017subject
Has Abstractpub_date
2009-06-05 00:00:00pages
358-62issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(09)00698-6journal_volume
383pub_type
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