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N. Shimada, K. Ohno-Matsui, J. Wang, T. Yoshida, M. Mochizuki, I. Morita; Reduced Retinal and Choroidal Neovascularization in Cathepsin L Gene-Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):529.
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© ARVO (1962-2015); The Authors (2016-present)
Recent studies using animal models have demonstrated that bone marrow-derived endothelial progenitor cells (EPCs) contributed to the retinal and choroidal neovascularization. It has also been reported that the protease Cathepsin L plays an important role for EPC-mediated neovascularization. To provide a novel therapeutic strategy targeting EPCs, we examined whether retinal and choroidal neovasucularization were decreased in Cathepsin L-deficient mouse.
Oxygen-induced ischemic retinopathy (OIR) and choroidal neovascularization (CNV) were induced in wild (c57BL6) mice and Cathepsin L-deficient mice. Mice with OIR were sacrificed at P17 and mice with CNV were sacrificed 2 weeks after laser injury. Serial sections were made from the eyeball and the area of neovascularization was analyzed using image analysis software.
In OIR model, Cathepsin L-deficient mice had significantly less retinal neovascularization than wild mice (22.7% of wild mice (P<0.01)). In CNV model, Cathepsin L-deficient mice also had significantly less CNV than wild mice (18.3% of wild mice (P<0.01)).
Cathepsin L deficiency resulted in a reduced neovascularization in OIR and CNV model. The results suggest that Cathepsin L plays a critical role in the development of retinal and choroidal neovascularization, and the inhibition of Cathepsin L might be a novel therapeutic target for intraocular neovascularization.
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