Abstract
Purpose: :
Age-related macular regeneration is characterized by intraocular neovascularization. The ideal goal of the treatment is to prevent the invasion of new vessels into the avascular tissue through a matrix barrier. The purpose of this study was to determine the role of cathepsin L, a matrix degrading enzyme, in choroidal neovascularization (CNV).
Methods: :
Laser irradiation was performed to induce CNV in wild type C57BL mice which received bone marrow transplantation from cathepsin L gene-deficient mice or wild type mice. Two weeks after laser irradiation, serial sections were cut from the enucleated eyeball and the area of CNV was measured. To identify the cathepsin L-expressed cells during the CNV development, the sections were immunocytochemically analyzed using different cell markers.
Results: :
Transplantation of bone marrow from cathepsin L-deficient mice into wild type mice significantly reduced the degree of CNV. Immunohistochemical analyses demonstrated that VE cadherin-positive endothelial progenitor cells (EPCs), but not CD43-positive or Iba-1 positive cells, were the major cells contributing to the production of cathepsin L.
Conclusions: :
These data indicate that cathepsin L-expressed EPCs from bone marrow plays a critical role in CNV and suggest a potential therapeutic approach of targeting cathepsin L for CNV.
Keywords: choroid: neovascularization