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Degree

Master of Sciences, Case Western Reserve University, Clinical Research, 2009.

Abstract

Proliferative diabetic retinopathy (PDR) is one of the leading causes of visual loss in the developing world. Retinal ischemia resulting from capillary occlusion is the initiating step for pre-retinal neovascularization. There is emerging evidence suggesting that circulating endothelial progenitor cells participate in post-natal neoangiogenesis and specifically that CD34+ CD45- endothelial colony-forming cells (ECFCs) may have unique characteristics to form functional vessels de novo. The purpose of this study was to determine whether PDR ECFCs are impaired in their ability to repair damaged retinal vasculature. Mononuclear cells isolated from PDR patients demonstrated a two-fold increase in circulating CD34+ CD45- ECFCs compared to controls. However, PDR ECFCs were impaired in migrating towards SDF-1 and human sera and were unable to incorporate with human retinal endothelial cells into vascular tubes. PDR ECFCs expressed higher levels of thrombospondin-1 and TIMP-3. Our results suggest that ECFCs in PDR patients are mobilized into the circulation but are defective in their ability to migrate and repair damaged capillary endothelium. This may result from derangements in the expression of angiogenesis inhibitors such as thrombospondin-1 and TIMP-3.

Subject Headings

Biomedical research

Keywords

Diabetic retinopathy; Proliferative diabetic retinopathy; Diabetes; Endothelial progenitor cells; stem cells; Endothelial colony forming cells

Committee / Advisors

Bela Anand-Apte, MD, PhD (Advisor)
Jonathan Sears, MD (Committee Chair)
Serpil Erzurum, MD (Committee Member)
Barbara Cromer, MD (Committee Member)

Pages

54p.

Document number: case1238452739
Permalink: http://rave.ohiolink.edu/etdc/view?acc_num=case1238452739

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