May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Peroxiredoxin6–Deficient Mouse Lens Epithelial Cells Exhibit an Increased Susceptibility to Hypergylycemia Induced Apoptosis
Author Affiliations & Notes
  • T. Miyazawa
    Department of Ophthalmology, University of Fukui, Yoshida–gun, Japan
  • E. Kubo
    Department of Ophthalmology, University of Fukui, Yoshida–gun, Japan
  • N. Fatma
    Department of Ophthalmology, University of Nebraska Medical Center, Omaha, NE
  • Y. Kumamoto
    Department of Ophthalmology, University of Fukui, Yoshida–gun, Japan
  • D.P. Singh
    Department of Ophthalmology, University of Nebraska Medical Center, Omaha, NE
  • Y. Akagi
    Department of Ophthalmology, University of Fukui, Yoshida–gun, Japan
  • Footnotes
    Commercial Relationships  T. Miyazawa, None; E. Kubo, None; N. Fatma, None; Y. Kumamoto, None; D.P. Singh, None; Y. Akagi, None.
  • Footnotes
    Support  NIH Grant RO1 13394 and Grants–in–Aid CategoryA;16689027
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3859. doi:
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      T. Miyazawa, E. Kubo, N. Fatma, Y. Kumamoto, D.P. Singh, Y. Akagi; Peroxiredoxin6–Deficient Mouse Lens Epithelial Cells Exhibit an Increased Susceptibility to Hypergylycemia Induced Apoptosis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3859.

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

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Abstract

Abstract: : Purpose:Cataract is a major complication in diabetic patients. There is now sufficient evidence implicating oxidative stress as a key factor in the etiology and progression of diabetic cataract. Peroxiredoxin 6 (Prdx6), an antioxidant protein, provides cyto– protection from oxidative stress. In this study, we demonstrated the ability of Prdx6 to protect eye lenses and/or LECs against hyperglycemia–induced stress. To this end, we utilized cultured lenses and lens epithelial cells (LECs) from normal and Prdx6 knock out mice. Methods:Lenses were isolated from Prdx6–/– and Prdx6+/+ mice, and LECs were generated. LECs were cultured in 5 and 50mM D–glucose with or without Prdx6 addition to assess its protective effect. Real–time PCR and Western analysis were done to monitor Prdx6 expression in LEC facing hyperglycemic stress. MTS and TUNEL assays were used to assess cell viability and to detect apoptotic cell death. Reactive oxygen species (ROS) in LECs and LECs facing hyperglycemia were monitored with H2DCFH–DA dye and compared. Results:LECs either from Prdx6–/– or Prdx6+/+ mice survived and grew in DMEM + 10% serum. Prdx6–/– cells were more susceptible to hyperglycemia induced stress (50 mM) and showed higher level of ROS, and underwent apoptosis. Supply of Prdx6 to Prdx6–/– cells could overcome from hyperglycemia– induced damage. Prdx6+/+ cells facing hyperglycemic stress showed diminished expression pattern of Prdx6. Conclusions:Present findings emphasize the importance of Prdx6 in cellular defense against hyperglycemia–induced damage, and this definition of protective efficacy of Prdx6 during hyperglycemia may help in considering the molecule’s usefulness in preventing diabetic complications.

Keywords: cataract • antioxidants • apoptosis/cell death 
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