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N. Shimada, K. Ohno-Matsui, A. Kojima, M. Mochizuki, I. Morita; Inhibition of Cathepsin L Causes a Reduced Neovascularization in the Retina and Choroid. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1753.
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Recent studies have demonstrated that endothelial progenitor cells (EPCs) were recruited to the retina and contributed to the retinal and choroidal neovascularization in a murine model. Interestingly, it has also been shown that the protease cathepsin L has a critical role for EPC-mediated neovascularization (C Urbich, Nat Med 2004). To offer a novel therapeutic strategy targeting EPCs, we examined whether retinal and choroidal neovasucularization were decreased by inhibition of cathepsin L.
Mice with oxygen-induced ischemic retinopathy (OIR) or with choroidal neovascularization (CNV) received periocular injection of cathepsin L inhibitor or vehicle only. Mice with OIR were sacrificed at P17 and mice with CNV were sacrificed 2 weeks after laser irradiation. Serial sections were made from the eyeball and the area of neovascularization was analyzed using image analysis software.
In OIR, mice treated with 400 µM or 40 µM cathepsin L inhibitor had significantly less retinal neovascularization than did vehicle-treated mice (49.6% and 26.0% of vehicle-treated mice (P<0.01)). In CNV model, mice treated with 400 µM or 40 µM cathepsin L inhibitor also had significantly less CNV than did vehicle-treated mice (40.8% and 21.1% of vehicle-treated mice (P<0.01)).
Inhibition of cathepsin L causes 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 cathepsin L might be a novel therapeutic target for intraocular pathological neovascularization.
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