April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Akt1 Accelerates Oxidative Apoptosis in HLE-PC Cells
Author Affiliations & Notes
  • L. Zhang
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
    College of Life Sciences, Hunan Normal University, Changsha, China
  • X. Zeng
    College of Life Sciences, Hunan Normal University, Changsha, China
  • S. Sun
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
    College of Life Sciences, Hunan Normal University, Changsha, China
  • L. Xiao
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
  • L. Gong
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
  • M. Deng
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
  • J. Liu
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
  • H. Ma
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
  • D. W. Li
    Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska
    College of Life Sciences, Hunan Normal University, Changsha, China
  • Footnotes
    Commercial Relationships  L. Zhang, None; X. Zeng, None; S. Sun, None; L. Xiao, None; L. Gong, None; M. Deng, None; J. Liu, None; H. Ma, None; D.W. Li, None.
  • Footnotes
    Support  NIH Grant EY15765 and EY18380
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3822. doi:https://doi.org/
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    • Get Citation

      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. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : 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.

Methods: : 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.

Results: : 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.

Conclusions: : Akt1 overexpression accelerates oxidative stress-induced apoptosis in HLE-PC cells.

Keywords: cataract • apoptosis/cell death • oxidation/oxidative or free radical damage 
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