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L. Zhang, X. Zeng, S. Sun, L. Xiao, L. Gong, M. Deng, J. Liu, H. Ma, D. W. Li; Akt1 Accelerates Oxidative Apoptosis in HLE-PC Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3822.
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Akt signaling pathway plays a very important role in mediating lens differentiation, development and stress-induced pathogenesis. Oxidative stress has been shown to play a role in cataractogenesis and one of the mechanisms for oxidative stress to induce cataractogenesis occur through induction of lens epithelial cell apoptosis. Thus, one of the mechanisms for Akt to promote survival is to prevent stress-induced apoptosis. In the present study, we have examined the role of Akt1 in regulating oxidative stress-induced apoptosis.
A stable system to generate hydrogen peroxide was utilized for the oxidative insult of various types of lens epithelial cells. Both vector and Akt1 transfected human lens epithelial cells were established for this study. Cell flow cytometry and MTT assays were used for detection of apoptosis. Western blot analysis was used to examine the activation of Akt1 and determine the expression patterns of the apoptosis-related genes including p53 and members of the Blc-2 family.
Hydrogen peroxide induces apoptosis in both vector- and Akt1- transfected cells. However, the apoptosis rate in Akt-transfected stable line is higher than that in vector transfected cells. Associated with this differentially apoptotic process, we observed that the tumor suppressor, p53 is phosphorylated at Ser-15 and Ser-37 much strongly in Akt1-transfected cells than in vector-transfected cells. The p53 target genes, both Bak and Bax are up-regulated more in Akt1-transfected cells than in vector-transfected cells.
Akt1 overexpression accelerates oxidative stress-induced apoptosis in HLE-PC cells.
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