May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Reduced Retinal and Choroidal Neovascularization in Cathepsin L Gene-Deficient Mice
Author Affiliations & Notes
  • N. Shimada
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Ophthalmology,
  • K. Ohno-Matsui
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Ophthalmology,
  • J. Wang
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Ophthalmology,
  • T. Yoshida
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Ophthalmology,
  • M. Mochizuki
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Ophthalmology,
  • I. Morita
    Tokyo Medical & Dental Univ, Tokyo, Japan
    Cellular Physiological Chemistry,
  • Footnotes
    Commercial Relationships  N. Shimada, None; K. Ohno-Matsui, None; J. Wang, None; T. Yoshida, None; M. Mochizuki, None; I. Morita, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 529. doi:https://doi.org/
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    • Get Citation

      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. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : 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.

Methods: : 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.

Results: : 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)).

Conclusions: : 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.

Keywords: choroid: neovascularization • retinopathy of prematurity • retinal neovascularization 
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