Front Row: Quteba Ebrahem, M.D., Bela Anand-Apte, M.B.B.S., Ph.D., and Nina Moore, Ph.D. Back Row: Phil Klenotic, Ph.D., and Jian Hua Qi, Ph.D.
Director: Bela Anand-Apte, Ph.D., M.B.B.S.
Department of Ophthalmic Research
Cole Eye Institute
9500 Euclid Avenue, i32
Office telephone: 216.445.9739
Goals and projects:
Ocular Neovascularization Regulated by Extracellular Matrix
The clinical significance of ocular angiogenesis is enormous, due to the fact that in the Western hemisphere, retinal neovascularization resulting from diabetic retinopathy is the most common cause of new blindness in young patients. Choroidal neovascularization (CNV) is the chief cause of severe and irreversible loss of vision in elderly patients.
Much progress has been made in the field of angiogenesis research in recent years, fueled by the hypothesis that inhibition of angiogenesis would be a useful strategy to treat cancers. However, there are a number of other diseases in which pathologic angiogenesis plays a role. Retinal neovascularization involves the development of sprouts from retinal vessels, which usually penetrates the inner limiting membrane (ILM) and grows into the vitreous. Retinal neovascularization is observed in ischaemic retinopathies such as diabetic retinopathy, retinopathy of prematurity, central vein occlusion and branch retinal vein occlusion. Choroidal neovascularization (CNV) refers to the formation of new vessels in the subretinal or sub RPE space, which arises from the choriocapillaris. CNV is seen in ocular diseases such as AMD, presumed ocular histoplasmosis, high myopia and angioid streaks.
The broad, long-term goal of the laboratory is to gain an understanding of the mechanism(s) by which alterations in matrix integrity may regulate ocular neovascularization. We are continuing our studies on the role of Tissue Inhibitor of Metalloproteinases-3 in the regulation of choroidal neovascularization and are exploring its potential as a therapeutic agent. We have also identified a novel ADAM-TS like molecule which is expressed in the retina and may play a role in angiogenesis. We are attempting to identify other novel endogenous inducers and inhibitors of angiogenesis to understand the basic biology of neovascularization with a final goal of designing therapeutic approaches to combat this process in disease states.
Our ultimate goal is the prevention and/or reversal of this process in an effort to control the devastating consequences of ocular neovascularization.