May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Retinal Vessel Remodeling During Hyperoxia
Author Affiliations & Notes
  • L. Pham
    Ophthalmology,
    Doheny Eye Institute and the Keck School of Medicine, University of Southern California, Los Angeles, CA
  • C.K. Chan
    Pathology,
    Doheny Eye Institute and the Keck School of Medicine, University of Southern California, Los Angeles, CA
  • C. Spee
    Ophthalmology,
    Doheny Eye Institute and the Keck School of Medicine, University of Southern California, Los Angeles, CA
  • S.J. Ryan
    Ophthalmology,
    Doheny Eye Institute and the Keck School of Medicine, University of Southern California, Los Angeles, CA
  • D.R. Hinton
    Pathology and Ophthalmology,
    Doheny Eye Institute and the Keck School of Medicine, University of Southern California, Los Angeles, CA
  • Footnotes
    Commercial Relationships  L. Pham, None; C.K. Chan, None; C. Spee, None; S.J. Ryan, None; D.R. Hinton, None.
  • Footnotes
    Support  NIH grants EY03040 and EY01545, Research to Prevent Blindness, Arnold and Mabel Beckman Foundation
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1874. doi:
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      L. Pham, C.K. Chan, C. Spee, S.J. Ryan, D.R. Hinton; Retinal Vessel Remodeling During Hyperoxia . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1874.

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

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Abstract

Abstract: : Purpose: Vaso–obliteration plays a key role in the pathogenesis of several forms of retinal angiogenesis. The purpose of this study was to determine the expression levels of apoptotic genes in a murine model of hyperoxia–induced retinal vaso–obliteration. Methods: To induce vessel regression, C57BL/6J neonatal mice (p7) were exposed to 75% oxygen for 5 days. The pups were euthanized, and their eyes enucleated and fixed in 4% paraformaldehyde overnight. The posterior pole of each eye was dissected and apoptosis was evaluated using a TUNEL assay. Retinas were flat–mounted and the extent of hyperoxia–induced apoptosis was visualized by confocal microscopy. To characterize gene expression during retinal vessel regression, total RNA was isolated from posterior poles of each animal subjected to the hyperoxia model at 0, 6, 12, 24, 48, 72, and 96 h. Hyperoxic regulation of caspase–3, –8, and –9, and Bcl–2 were evaluated using quantitative real–time RT–PCR. Results: The TUNEL assay revealed predominant endothelial cell–specific apoptosis in C57BL/6J mice exposed to 5 days hyperoxia. Evaluation of gene expression using real time RT–PCR showed a peak 1.4– and 2.4–fold increased expression of caspase–3 and –9 respectively following 12 h hyperoxia compared to 0 h (p < 0.01). In contrast, caspase–8 expression did not change significantly throughout the entire time course of hyperoxia. However, Bcl–2 mRNA levels became steadily elevated, reaching over 2–fold increased expression at 48 h hyperoxia compared to 0h (p < 0.0001). Conclusion: This data indicates that hyperoxia–induced vessel remodeling involves the regulation of both pro– and anti–apoptotic factors. In fact, caspase–3 and –9 may play a more important role in hyperoxia–induced vaso–obliteration compared to caspase–8. Moreover, later increased expression of Bcl–2 may be a protective response to hyperoxic insult. Further elucidation and modulation of endothelial apoptosis may provide valuable pharmacologic targets toward ischemia–induced retinopathies such as diabetic retinopathy and retinopathy of prematurity.

Keywords: cell death/apoptosis • diabetic retinopathy • retina 
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