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Yue Xu, Qiaochu Cheng, Boyu Yang, Shanshan Yu, Fan Xu, Lin Lu, Xiaoling Liang; Increased sCD200 Levels in Vitreous of Patients With Proliferative Diabetic Retinopathy and Its Correlation With VEGF and Proinflammatory Cytokines. Invest. Ophthalmol. Vis. Sci. 2015;56(11):6565-6572. doi: 10.1167/iovs.15-16854.
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The purpose of this study was to determine the levels of sCD200 expression in the vitreous of proliferative diabetic retinopathy (PDR) patients and to clarify its correlation with different vitreoretinal conditions, VEGF and its receptors, and proinflammatory cytokines.
The expression of sCD200, VEGF and its receptors, and other proinflammatory cytokines were examined by using ELISA. Clinical stratification was performed on patients with different vitreoretinal conditions for correlation analysis.
The vitreous levels of sCD200 were significantly higher in the PDR group (182.2 ± 17.63 pg/mL) compared with those in the control group (56.86 ± 6.573 pg/mL; P < 0.0001). The venous blood levels of sCD200 were 26.71 ± 4.32 pg/mL in the PDR group and 19.94 ± 3.87 pg/mL in the control group (P = 0.2614). The vitreous levels of sCD200 were significantly elevated in PDR patients with diabetic macular edema (DME; 266.9 ± 28.82 pg/mL) or traction retinal detachment (TRD; 256.9 ± 34.50 pg/mL) compared with the PDR group without DME (136.9 ± 15.13 pg/mL; P < 0.0001) or TRD (146.9 ± 15.97 pg/mL; P = 0.0024). The vitreous levels of CCL2, CXCL4, CXCL9, CXCL10, VEGF, sVEGFR-1, sVEGFR-2, IL-6, IL-8, IL-10, and IL-18 were also elevated significantly in the PDR group. Statistical association was found between sCD200 levels and VEGF (r = 0.6566, P < 0.0001), sVEGFR-1 (r = 0.5574, P = 0.006), sVEGFR-2 (r = 0.3605, P = 0.0362), CCL-2 (r = 0.6001, P = 0.0002), IL-6 (r = 0.5704, P = 0.0004), IL-8 (r = 0.3712, P = 0.0307), and IL-10 (r = 0.3618, P = 0.0355).
Expression of sCD200 may contribute to retinal angiogenesis by interacting with VEGF-mediated inflammatory response and represents a potential therapeutic target for the patients with PDR.
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