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S. He, R. Kannan, J. Zhou, E. Wawrousek, M. Jin, S.J. Ryan, D.R. Hinton; Laser–Induced Choroidal Neovascularization in B Crystallin Knockout Mice . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5301.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: αB crystallin, an ubiquitous member of the small heat shock protein family, is induced by thermal stress and other environmental and pathological conditions such as UV radiation, hypoxia and ischemia. We investigated the role of αB crystallin in retinal injury by evaluating laser–induced choroidal neovascularization (CNV) in αB crystallin knockout mice and controls. Methods: αB crystallin knockout and wild type (wt) 129S3/SvJ mice were used in these studies. The mice were anesthetized with a mixture of ketamine/xylazine and the pupils were dilated with a single drop of 1% tropicamide. Laser photocoagulation (75 µm spot size, 0.05s duration, 130 mV) was performed to generate two laser spots in each eye surrounding the optic nerve. A bubble formed at a laser spot indicated rupture of the Bruch’s membrane. Fluorescent angiogram (FA) was performed on days 7 and day 14 post–laser exposure. The laser spots were evaluated for the presence of CNV on day 7 or day 17 after laser treatment by histology. Results: FA revealed no difference in fluorescein leakage between controls and knockout mice at one week post–laser; however, at d14 post–laser, leakage was significantly reduced (p<0.02) in αB crystallin knockout mice as compared to wt controls. Induction of CNV by laser photocoagulation was verified by histological examination in both groups; after 14d post–laser, the size of the CNV lesions was significantly decreased in αB knockout mice. Conclusions: Laser induced CNV is reduced in αB crystallin knockout mice compared to wt controls. The effect was found late in the course of CNV suggesting that survival of newly formed vessels may be affected.
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