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Whitney Greene, Teresa Burke, Gregory Bramblett, Heuy-Ching Hetty Wang; Inflammation and intraocular fibrosis in a rabbit model of penetrating injury to the posterior segment. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5815.
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© ARVO (1962-2015); The Authors (2016-present)
To establish a rabbit model of penetrating injury to the posterior segment as a platform to analyze pathological mechanisms and test potential therapeutics. Injury to the retina can lead to intraocular fibrosis and may cause vision loss. Although there have been numerous advances in surgical management to repair the retina, the continuous scarring in the eye after surgery eventually leads to severe vision loss or blindness. The contribution of inflammatory and fibrotic proteins to the pathology of intraocular fibrosis was examined in rabbits after penetrating eye injury
10 male Dutch Belted rabbits were divided into two groups (Table 1). Group A received penetrating eye injury and was terminated on Day 14. Group B received penetrating eye injury and was terminated on Day 28. While under anesthesia, posterior penetrating eye injury was induced in one eye with contralateral eye acting as the uninjured control. Injured and control eyes were examined by intraocular pressure measurement, indirect ophthalmoscope, fundus photography, and electroretinography once a week post –injury until the termination. Group A was euthanized on Day 14 to determine fibrosis at early phase of disease progression. Group B was euthanized on Day 28 to examine fibrosis at late phase of disease progression. Eyes were processed for histology and immunofluorescence labeling of fibrotic proteins alpha-smooth muscle actin and collagen I, and inflammatory proteins TGFb2, TNFa, VEGF, and GFAP.
Rabbits were examined at 0, 7, 14, 21, and 28 days post injury. Indirect ophthalmoscopy and fundus imaging detected fibrosis by day 14. Fibrotic membranes were visible at the site of the original injury. Immunofluorescence analysis detected alpha-smooth muscle actin and collagen I within fibrotic membranes. Inflammatory proteins TGFb2, TNFa, VEGF, and GFAP were also detected at elevated levels in injured eyes compared to uninjured control eyes.
These data show that ocular fibrosis can be detected within 14 days after initial injury. More severe fibrosis is detected at 28 days post-injury. Collagen I and alpha-smooth muscle actin were detected within fibrotic membranes. Inflammatory proteins were detected in both fibrotic membranes and surrounding tissues. Secretion of these factors from surrounding tissues after injury may contribute to pathology of intraocular fibrosis.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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