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D. Husain, E. Chou, E. Ahmed, N. Rahimi; Experimental Choroidal Neovascularization in c-Cbl Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2972.
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Activation of phospholipase C gamma1 (PLCgamma1) by vascular endothelial growth factor receptor-2 (VEGFR-2) is responsible for angiogenesis in vivo. Previous work has demonstrated that Casitas B-lineage lymphoma (c-Cbl) suppresses activation of PLC-gamma1 by ubiquitination-dependent manner and with it VEGF-mediated endothelial cell proliferation and tube formation. This study is designed to evaluate the role of c-Cbl in angiogenesis, by creating experiemental choroidal neovascularization (CNV) in c-Cbl knockout mice.
CNV was created using the laser photocoagulation method (Green laser, 50µ, 0.1 seconds, 200mw). 14 lesions were induced in the knockout mice and 18 lesions in control wild mice. These lesions were followed at days 7, 10, 14 and 21. Fundus photography and angiography was done to document size and leakage from the CNV in these lesions at each visit.
Leaking CNV were found in 10/14 (71%) lesions in the c-Cbl knockout mice as compared to 6/18 lesions (33%) in the control mice (p=0.03). Confluence was found in 6/14 (42%) lesions in c-Cbl knockout mice and 2/18 (11%) lesions in control mice (p=0.04). Fluorescein angiography of the lesions showed that they were progressively larger in size at the 4-week follow-up as compared to the earlier time points in the c-Cbl knockout mice.
We found that CNV lesions in the c-Cbl knockout mice were significantly more in number, more confluent and increased in size with time as compared to control wild type mice. This work for the first time demonstrates that c-Cbl play an inhibitory role in laser-induced CNV.
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