Duh Elia J, Yang Hoseong S, Haller Julia A, De Juan Eugene, Humayun Mark S, Gehlbach Peter, Melia Michele, Pieramici Dante, Harlan J B, Campochiaro Peter A, Zack Donald J
Department of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Am J Ophthalmol. 2004 Apr;137(4):668-74. doi: 10.1016/j.ajo.2003.11.015.
Pigment epithelium-derived factor (PEDF) has been demonstrated to suppress ocular angiogenesis in several animal models. In this study, we sought to measure the levels of PEDF and vascular endothelial growth factor (VEGF) in the vitreous of patients with and without ocular neovascular disorders.
Case-control study of patients undergoing intraocular surgery for a variety of neovascular and nonneovascular conditions.
Vitreous samples were collected from 65 eyes of 65 patients with no neovascular disorder (n = 24), choroidal neovascularization (n = 9), active proliferative diabetic retinopathy (n = 16), and inactive proliferative diabetic retinopathy (n = 16). The levels of VEGF and PEDF in these vitreous samples were determined by enzyme-linked immunosorbent assay.
The VEGF levels were at or below the level of detectability in the reference and choroidal neovascularization groups. The VEGF levels were significantly elevated in both the active and inactive PDR groups, and significantly higher in the active PDR group as compared with the inactive PDR group. The PEDF levels, which were present at relatively high concentrations in all groups, were higher in patients with active PDR compared with the control and choroidal neovascularization groups.
High levels of immunoreactive PEDF are present in the vitreous of individuals with or without ocular neovascularization, but PEDF levels are significantly higher in patients with active PDR compared with patients with choroidal neovascularization or nonneovascular retinal diseases. Although these results do not preclude the possibility that endogenous PEDF helps to modulate ocular neovascularization, they do not support ischemia-induced downregulation of PEDF as a mechanism for such modulation.
色素上皮衍生因子(PEDF)已在多种动物模型中被证明可抑制眼部血管生成。在本研究中,我们试图测量患有和未患有眼部新生血管疾病患者玻璃体内PEDF和血管内皮生长因子(VEGF)的水平。
对因各种新生血管和非新生血管疾病接受眼内手术的患者进行病例对照研究。
从65例患者的65只眼中收集玻璃体样本,这些患者包括无新生血管疾病者(n = 24)、脉络膜新生血管形成者(n = 9)、活动性增殖性糖尿病视网膜病变者(n = 16)和非活动性增殖性糖尿病视网膜病变者(n = 16)。通过酶联免疫吸附测定法测定这些玻璃体样本中VEGF和PEDF的水平。
参考组和脉络膜新生血管形成组的VEGF水平处于或低于可检测水平。活动性和非活动性增殖性糖尿病视网膜病变组的VEGF水平均显著升高,且活动性增殖性糖尿病视网膜病变组的VEGF水平显著高于非活动性增殖性糖尿病视网膜病变组。所有组中PEDF水平均相对较高,与对照组和脉络膜新生血管形成组相比,活动性增殖性糖尿病视网膜病变患者的PEDF水平更高。
无论有无眼部新生血管形成,个体玻璃体内均存在高水平的免疫反应性PEDF,但与脉络膜新生血管形成或非新生血管性视网膜疾病患者相比,活动性增殖性糖尿病视网膜病变患者的PEDF水平显著更高。虽然这些结果不排除内源性PEDF有助于调节眼部新生血管形成的可能性,但它们不支持缺血诱导的PEDF下调作为这种调节的机制。