April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
The Composition of Pathological Vessels and Changes in the ILM That Are Caused by Oxygen-Induced Retinopathy in Rats
Author Affiliations & Notes
  • M. M. Staniszewska
    Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts
  • X. Gu
    Alcon, Forth Worth, Texas
  • C. Romano
    Alcon, Forth Worth, Texas
  • A. Kazlauskas
    Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  M.M. Staniszewska, Alcon, F; X. Gu, Alcon, E; C. Romano, Alcon, E; A. Kazlauskas, Alcon, F.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 108. doi:
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      M. M. Staniszewska, X. Gu, C. Romano, A. Kazlauskas; The Composition of Pathological Vessels and Changes in the ILM That Are Caused by Oxygen-Induced Retinopathy in Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):108.

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

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Abstract

Purpose: : To characterize hypoxia-induced retinal pathology, with a particular emphasis on the inner limiting membrane (ILM) and the cellular composition of the pathological vasculature.

Methods: : We used the standard rat model of oxygen-induced retinopathy (OIR) in which newborn rats experience 14 successive 12 hr periods of 10% and 50% oxygen, followed by 6 days in room air. Control animals breathed room air for the entire period of time. The retinas were fixed, flat mounted and examined by either scanning electron microscopy, or confocal immunofluorescence with reagents that selectively recognized the following cell types: endothelial cells (isolectin IB4), pericytes (NG2), activated astrocytes (GFAP) and macrophage/microglia (CD11b).

Results: : The OIR protocol induced profound changes to the ILM. In control animals the surface of the ILM displayed a uniform polygonal pattern. While a similar pattern was present on the surface of the ILM from OIR animals, protuberant structures were also observed. Furthermore, the fibrillar structure of the ILM was compromised in OIR animals, and this change was likely to permit vitreal ingrowth of pathological neovessels. These vessels consisted of disorganized, 3-dimensional structures (tufts), located above the plane of the ILM, extending into the retina and connecting to vessels of the superficial layer. In addition, there were sheets of abnormal vessels that formed ridges on the surface of the ILM. While both types of pathological neovessels were primarily composed of endothelial cells, they also contained the following cell types, listed in descending order of abundance: pericytes>macrophage/microglia≥activated astrocytes.

Conclusions: : Hypoxia-induced retinopathy involved changes to the surface of the ILM and manifestation of pathological neovessels that consisted of at least 3 cell types other then endothelial cells. The observations implicate perturbation of the ILM and several non-endothelial cell types as potential contributors to proliferative retinopathies.

Keywords: neovascularization • diabetic retinopathy • retinopathy of prematurity 
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