Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia ; Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, P.O. Box 245, Riyadh 11411, Saudi Arabia.
J Diabetes Res. 2013;2013:539658. doi: 10.1155/2013/539658. Epub 2013 Mar 10.
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 (P < 0.001; 0.007; 0.001; <0.001, resp.). In contrast, PGE2 levels were significantly higher in nondiabetic patients compared with PDR patients (P < 0.001). There were significant correlations between levels of sVEGFR-2 versus SCF (r = 0.950, P < 0.001), sVEGFR-2 versus s-kit (r = 0.941, P < 0.001), and SCF versus s-kit (r = 0.970, P < 0.001). Our findings suggest that upregulation of VEGF, sVEGFR-2, SCF, and s-kit supports the contributions of angiogenesis and vasculogenesis in pathogenesis of PDR.
本研究旨在确定增生性糖尿病视网膜病变(PDR)患者玻璃体液中血管生成和内皮祖细胞动员(血管生成)因子的水平,并将其与临床疾病活动相关联。通过 ELISA 测量了 34 例 PDR 患者和 15 例非糖尿病患者玻璃体液样本中的血管内皮生长因子(VEGF)、可溶性血管内皮生长因子受体-2(sVEGFR-2)、干细胞因子(SCF)、可溶性 c-kit(s-kit)、内皮型一氧化氮合酶(eNOS)和前列腺素 E2(PGE2)水平。未检测到 eNOS。与静止性 PDR 和非糖尿病患者相比,活动性新生血管形成的 PDR 患者的 VEGF、sVEGFR-2、SCF 和 s-kit 水平显著升高(P<0.001;0.007;0.001;<0.001,分别)。相比之下,非糖尿病患者的 PGE2 水平明显高于 PDR 患者(P<0.001)。sVEGFR-2 与 SCF(r=0.950,P<0.001)、sVEGFR-2 与 s-kit(r=0.941,P<0.001)以及 SCF 与 s-kit(r=0.970,P<0.001)之间存在显著相关性。我们的研究结果表明,VEGF、sVEGFR-2、SCF 和 s-kit 的上调支持了血管生成和血管生成在 PDR 发病机制中的贡献。