| First Author | Jee HJ | Year | 2009 |
| Journal | Biochem Biophys Res Commun | Volume | 383 |
| Issue | 3 | Pages | 358-62 |
| PubMed ID | 19364500 | Mgi Jnum | J:149681 |
| Mgi Id | MGI:3848859 | Doi | 10.1016/j.bbrc.2009.04.017 |
| Citation | Jee HJ, et al. (2009) UV light induces premature senescence in Akt1-null mouse embryonic fibroblasts by increasing intracellular levels of ROS. Biochem Biophys Res Commun 383(3):358-62 |
| abstractText | 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. |
