Angiogenic and vasculogenic factors in the vitreous from patients with proliferative diabetic retinopathy.
Angiogenic and vasculogenic factors in the vitreous from patients with proliferative diabetic retinopathy.
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DOI：
10.1155/2013/539658
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发表时间：
2013
影响因子：
4.3
通讯作者：
Geboes K
中科院分区：
文献类型：
--
作者：
Abu El-Asrar AM;Nawaz MI;Kangave D;Mairaj Siddiquei M;Geboes K
本研究旨在测定增殖性糖尿病视网膜病变 (PDR) 患者玻璃体液中血管生成因子和内皮祖细胞动员（血管生成）因子的水平，并将其水平与临床疾病活动性相关联。通过 ELISA 检测 34 名 PDR 和 15 名非糖尿病患者的玻璃体样本中血管内皮生长因子 (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)、内皮一氧化氮合酶 (eNOS) 和前列腺素 E2 (PGE2) 水平。未检测到 eNOS。与静态 PDR 和非糖尿病患者相比，具有活动性新生血管形成的 PDR 中 VEGF、sVEGFR-2、SCF 和 s-kit 水平显着较高（P < 0.001；0.007；0.001；<0.001）。相反，非糖尿病患者的 PGE2 水平显着高于 PDR 患者（P < 0.001）。 sVEGFR-2 与 SCF 的水平（r = 0.950，P < 0.001）、sVEGFR-2 与 s-kit 的水平（r = 0.941，P < 0.001）以及 SCF 与 s-kit 的水平（r = 0.970，P < 0.001）之间存在显着相关性。我们的研究结果表明，VEGF、sVEGFR-2、SCF 和 s-kit 的上调支持血管生成和血管生成在 PDR 发病机制中的作用。
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.
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