May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Hepatocyte Growth Factor Protects RPE Cells against Oxidative Stress-induced Apoptosis
Author Affiliations & Notes
  • M.L. Jin
    Doheny Eye Institute, Los Angeles, CA, United States
  • R. Kannan
    Doheny Eye Institute, Los Angeles, CA, United States
  • S. He
    Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • S.J. Ryan
    Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • D.R. Hinton
    Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States
  • Footnotes
    Commercial Relationships  M.L. Jin, None; R. Kannan, None; S. He, None; S.J. Ryan, None; D.R. Hinton, None.
  • Footnotes
    Support  EY02061, EY03040 and grants from Research to Prevent Blindness and the Arnold & Mabel Foundation.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1632. doi:
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      M.L. Jin, R. Kannan, S. He, S.J. Ryan, D.R. Hinton; Hepatocyte Growth Factor Protects RPE Cells against Oxidative Stress-induced Apoptosis . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1632.

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

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Abstract

Abstract: : Purpose: Oxidative damage to retinal pigment epithelial (RPE) cells has been implicated as a causative factor in the development of age-related macular degeneration. The ability of hepatocyte growth factor (HGF) to protect RPE cells from oxidative stress has not been elucidated. In this study, we investigated the effect of HGF on RPE cells in glutathione (GSH) depletion-induced oxidative injury. Methods: RPE cells were pretreated with HGF for 24 hrs (20ng/ml), and treated further with the GSH synthesis inhibitor DL-buthionine-(S,R)-sulfoximine (BSO) for 24 hrs (200uM). Apoptosis was measured by TUNEL assay. Intracellular GSH and lipid peroxides (LPO) were also measured. Results: Treatment for 24 hours with BSO resulted in a 90% decrease of intracellular GSH, a marked increase in LPO formation, and RPE cell apoptosis. HGF (20ng/ml) effectively inhibited BSO-induced apoptosis (~45%). LPO production was also considerablely reduced by HGF pretreatment. Intracellular GSH was increased 2 fold by HGF compared to BSO treated cells. Conclusions: Our findings support the contention that HGF protects RPE cells against oxidant stress induced cell damage and apoptosis.

Keywords: age-related macular degeneration • oxidation/oxidative or free radical damage • retinal pigment epithelium 
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