April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Nrf2 Modulates Oxidative Stress, Inflammation, and Neurovascular Injury in Retinal Ischemia-reperfusion
Yanhong Wei; Junsong Gong; Takeshi Yoshida; Rajesh Thimmulappa; Shyam Biswal; Elia J. Duh
Author Affiliations & Notes
  • Yanhong Wei
    Wilmer Eye Institute, School of Medicine,
    Johns Hopkins University, Baltimore, Maryland
  • Junsong Gong
    Wilmer Eye Institute, School of Medicine,
    Johns Hopkins University, Baltimore, Maryland
  • Takeshi Yoshida
    Wilmer Eye Institute, School of Medicine,
    Johns Hopkins University, Baltimore, Maryland
  • Rajesh Thimmulappa
    Environmental Health Sciences, Bloomberg School of Public Health,
    Johns Hopkins University, Baltimore, Maryland
  • Shyam Biswal
    Environmental Health Sciences, Bloomberg School of Public Health,
    Johns Hopkins University, Baltimore, Maryland
  • Elia J. Duh
    Wilmer Eye Institute, School of Medicine,
    Johns Hopkins University, Baltimore, Maryland
  • Footnotes
    Commercial Relationships  Yanhong Wei, None; Junsong Gong, None; Takeshi Yoshida, None; Rajesh Thimmulappa, None; Shyam Biswal, None; Elia J. Duh, None
  • Footnotes
    Support  Funds from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 6060. doi:
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      Yanhong Wei, Junsong Gong, Takeshi Yoshida, Rajesh Thimmulappa, Shyam Biswal, Elia J. Duh; Nrf2 Modulates Oxidative Stress, Inflammation, and Neurovascular Injury in Retinal Ischemia-reperfusion. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6060.

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Abstract

Purpose: : Retinal ischemia-reperfusion (I/R) involves extensive increase in reactive oxygen species as well as pro-inflammatory changes, with subsequent neuronal and vascular degeneration. Nrf2 has a well-known cytoprotective role in many tissues, although its function in the retina is less clear. The purpose of this study is to investigate the possible role of Nrf2 in retinal I/R injury using Nrf2-deficient mice.

Methods: : Retinal I/R injury was induced by elevating the intraocular pressure (IOP), and reperfusion was established immediately afterward. Dihydroethidium (DHE) staining and biochemical assay using lucigenin were used for superoxide measurement. Histological analysis, cell count in the ganglion cell layer, and apoptotic DNA cleavage ELISA were performed after 48 hours of I/R injury. Inflammatory gene expression was assessed by real-time PCR. Capillary degeneration was quantified in retinas 8 days after I/R.

Results: : I/R resulted in an increase in retinal levels of superoxide and pro-inflammatory mediators in Nrf2 +/+ mice, an effect which was accentuated in Nrf2 -/- mice. Leukocyte infiltration of the retina and vitreous, loss of cells in the ganglion cell layer, and retinal capillary degeneration were markedly accentuated by I/R in Nrf2 -/- mice as compared to wild-type.

Conclusions: : These studies indicate that Nrf2 is an important factor in modulating the retinal response to ischemia-reperfusion injury.

Keywords: ischemia • inflammation • oxidation/oxidative or free radical damage 
© 2011, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2024 Association for Research in Vision and Ophthalmology.
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