Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2013 (2013), Article ID 539658, 9 pages
Research Article

Angiogenic and Vasculogenic Factors in the Vitreous from Patients with Proliferative Diabetic Retinopathy

1Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia
2Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, P.O. Box 245, Riyadh 11411, Saudi Arabia
3Laboratory of Histochemistry and Cytochemistry, University of Leuven, Belgium

Received 22 December 2012; Accepted 12 February 2013

Academic Editor: Ghulam Mohammad

Copyright © 2013 Ahmed M. Abu El-Asrar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study was conducted to determine levels of angiogenic and endothelial progenitor cell mobilizing (vasculogenic) factors in vitreous fluid from proliferative diabetic retinopathy (PDR) patients and correlate their levels with clinical disease activity. Vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor receptor-2 (sVEGFR-2), stem cell factor (SCF), soluble c-kit (s-kit), endothelial nitric oxide synthase (eNOS), and prostaglandin E2 (PGE2) levels were measured by ELISA in vitreous samples from 34 PDR and 15 nondiabetic patients. eNOS was not detected. VEGF, sVEGFR-2, SCF, and s-kit levels were significantly higher in PDR with active neovascularization compared with quiescent PDR and nondiabetic patients ( ; 0.007; 0.001; , resp.). In contrast, PGE2 levels were significantly higher in nondiabetic patients compared with PDR patients ( ). There were significant correlations between levels of sVEGFR-2 versus SCF ( , ), sVEGFR-2 versus s-kit ( , ), and SCF versus s-kit ( , ). Our findings suggest that upregulation of VEGF, sVEGFR-2, SCF, and s-kit supports the contributions of angiogenesis and vasculogenesis in pathogenesis of PDR.