May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Estrogen Receptor ß May Protect Against Oxidant Injury in Rpe Cells
Author Affiliations & Notes
  • S. Elliot
    Medicine, Miller School of Medicine, Miami, FL
  • P. Catanuto
    Medicine, Miller School of Medicine, Miami, FL
  • D. Espinosa–Heidmann
    Opthalmology, Bascom Palmer Eye Institute, Miami, FL
  • P. Fernandez
    Medicine, Miller School of Medicine, Miami, FL
  • K. Korach
    National Institutes of Environmental Health Sciences, Research Triangle Park, NC
  • S. Cousins
    Duke Center for Macula Diseases, Duke University Eye Center, Durham, NC
  • Footnotes
    Commercial Relationships  S. Elliot, None; P. Catanuto, None; D. Espinosa–Heidmann, None; P. Fernandez, None; K. Korach, None; S. Cousins, None.
  • Footnotes
    Support  NIH Grant EY014477
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1383. doi:
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      S. Elliot, P. Catanuto, D. Espinosa–Heidmann, P. Fernandez, K. Korach, S. Cousins; Estrogen Receptor ß May Protect Against Oxidant Injury in Rpe Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1383.

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

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Purpose: : Age–related macular degeneration (AMD) demonstrates accumulation of specific lipid–rich deposits and extracellular matrix molecules under the retinal pigmented epithelium (RPE). Recent studies have shown that polymorphisms in complement factor H predispose patients to AMD, however other triggering events are necessary. In women, a decline in estrogen action during aging may be one such event. To determine the role of estrogens in AMD, RPE cells were isolated from estrogen receptor knockout mice (ERKO) that received either normal chow or a high fat diet and blue light mimicking oxidant injury.

Methods: : RPE cells were isolated from 14 month old ERKO (ERKOα and ERKOß) mice and their wildtype littermates. All groups of mice were fed either a high fat diet and exposed to blue light (in vivo injury model) or normal chow. To determine whether the cells retained their in vivo phenotype, immunohistochemistry for ZO1, cytokeratin 8 and RPE65 was performed. Zymography was performed for analysis of MMP–2 activity. RNA was collected and microarrays performed.

Results: : Immunohistochemistry revealed that established markers of RPE cells were retained in vitro. RPE cells isolated from ERKOß mice and exposed to transient injury in vitro had a greater decrease in MMP–2 activity than cells isolated from ERKOα mice. RPE cells isolated from ERKOß mice injured in vivo had less MMP–2 activity than wildtype controls and less baseline activity compared to ERKOα cells. Microarray analysis of mouse cells injured in vivo revealed a significant increase in collagen mRNA only in ERKOß cells.

Conclusions: : It appears that estrogen receptor ß may play a role in protection against oxidant injury mediated–MMP–2 activity decrease and collagen increase. Since mouse RPE cells can be isolated, and maintained in culture while retaining their in vivo phenotype, they provide a useful tool for studying the mechanisms behind the pathogenesis of AMD.

Keywords: age-related macular degeneration • retinal pigment epithelium 

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