Izuta Hiroshi, Chikaraishi Yuichi, Adachi Tetsuo, Shimazawa Masamitsu, Sugiyama Tetsuya, Ikeda Tsunehiko, Hara Hideaki
Department of Biofunctional Evaluation, Molecular Pharmacology, Gifu Pharmaceutical University, Mitahora-higashi, Japan.
Mol Vis. 2009 Dec 10;15:2663-72.
To evaluate the relationship between vascular endothelial growth factor (VEGF) and extracellular superoxide dismutase (EC-SOD) in vitreous body and serum in patients with proliferative diabetic retinopathy (PDR), and investigate the role of EC-SOD in PDR by evaluating its angiostatic effect, using an in vitro angiogenesis model. To investigate the role of EC-SOD in PDR by evaluating its angiostatic effect, using an in vitro angiogenesis model.
EC-SOD and VEGF concentrations in vitreous and serum samples from PDR and macular hole (MH) were measured by ELISA. The effects of EC-SOD on VEGF-induced proliferation, migration, and tube formation were evaluated using human umbilical vein endothelial cells (HUVECs). Moreover, the effects of EC-SOD on VEGF-induced proliferation and migration were evaluated in HUVECs and primary normal human retinal microvascular endothelial cells.
Intravitreal concentrations of EC-SOD were significantly higher (p<0.01) in PDR (58.0+/-23.8 ng/ml, mean+/-SD) than in MH (29.3+/-6.6 ng/ml). Intravitreal concentrations of VEGF were dramatically higher (p<0.01) in PDR (798.2+/-882.7 pg/ml) than in MH (17.7+/-15.5 pg/ml). The serum concentrations of EC-SOD and VEGF did not differ between the two patient groups. The vitreous concentrations of VEGF correlated with those of EC-SOD in all patients (rs=0.61, p<0.001). In HUVECs, EC-SOD at 100 ng/ml significantly suppressed VEGF-induced proliferation and tube formation, but not VEGF-induced migration.
EC-SOD was increased together with VEGF in the vitreous body from PDR patients, suggesting that EC-SOD may play a pivotal role in the pathogenesis of angiogenesis.
评估增殖性糖尿病视网膜病变（PDR）患者玻璃体和血清中血管内皮生长因子（VEGF）与细胞外超氧化物歧化酶（EC-SOD）之间的关系，并通过体外血管生成模型评估EC-SOD的血管生成抑制作用，以研究其在PDR中的作用。通过体外血管生成模型评估EC-SOD的血管生成抑制作用，以研究其在PDR中的作用。
采用酶联免疫吸附测定法（ELISA）检测PDR患者和黄斑裂孔（MH）患者玻璃体及血清样本中EC-SOD和VEGF的浓度。使用人脐静脉内皮细胞（HUVECs）评估EC-SOD对VEGF诱导的增殖、迁移和血管生成的影响。此外，在HUVECs和原代正常人视网膜微血管内皮细胞中评估EC-SOD对VEGF诱导的增殖和迁移的影响。
PDR患者玻璃体中EC-SOD的浓度（58.0±23.8 ng/ml，平均值±标准差）显著高于MH患者（29.3±6.6 ng/ml，p<0.01）。PDR患者玻璃体中VEGF的浓度（798.2±882.7 pg/ml）显著高于MH患者（17.7±15.5 pg/ml，p<0.01）。两组患者血清中EC-SOD和VEGF的浓度无差异。所有患者玻璃体中VEGF的浓度与EC-SOD的浓度相关（rs=0.61，p<0.001）。在HUVECs中，100 ng/ml的EC-SOD显著抑制VEGF诱导的增殖和血管生成，但不抑制VEGF诱导的迁移。
PDR患者玻璃体中EC-SOD与VEGF同时升高，提示EC-SOD可能在血管生成的发病机制中起关键作用。
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