增殖性糖尿病视网膜病变患者视网膜前膜中的apelin
Apelin in epiretinal membranes of patients with proliferative diabetic retinopathy.
作者信息
Lu Qiang, Ma Yan, Xu Yong-Sheng, Jiang Yan-Rong
机构信息
Department of Ophthalmology, People's Hospital, Peking University, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, Beijing, China ; Department of Ophthalmology, Inner Mongolia People's Hospital, Huhhot, China.
Department of Ophthalmology, People's Hospital, Peking University, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, Beijing, China ; Department of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
出版信息
Mol Vis. 2014 Jul 31;20:1122-31. eCollection 2014.
PURPOSE
Formation of epiretinal membranes (ERMs) in the posterior fundus results in visual impairment. ERMs have been associated with numerous clinical conditions, including proliferative diabetic retinopathy (PDR), a neovascular disease. Apelin has been identified as a novel angiogenesis contributor. The aim of this study was to investigate the correlation between apelin and ERMs after PDR.
METHODS
ERM samples were obtained by vitrectomy from 12 subjects with PDR (aged 57±6 years; duration of diabetes 16±7 years), and 12 subjects with idiopathic ERM (aged 68±5 years). The samples were processed for immunohistochemistry and reverse transcription-PCR (RT-PCR). We also analyzed samples from patients with PDR who received an intravitreal injection of bevacizumab (IVB) before vitrectomy.
RESULTS
The mRNA expression of apelin was significantly higher in the PDR ERMs than in the idiopathic ERMs. Accordingly, immunohistochemical analysis revealed strong expression of apelin in all eight PDR ERMs without IVB, and was double-labeled with glial fibrillary acidic protein antibody (GFAP), platelet endothelial cell adhesion molecule-1 (CD31), cytokeratin (CK) and vascular endothelial growth factor (VEGF) but not with fibronectin. They were mainly located in the adventitia. In contrast, the expression of apelin was lower in the PDR ERMs after IVB and the idiopathic ERMs.
CONCLUSIONS
The results showed that apelin was involved in the formation of ERMs and promoted the formation of adventitia, including glial, endothelial, and RPE cells. Bevacizumab blocked the expression of apelin and regressed gliosis and angiogenesis.
目的
眼底后部视网膜前膜（ERM）的形成会导致视力损害。ERM与多种临床病症相关，包括增殖性糖尿病视网膜病变（PDR），一种新生血管疾病。Apelin已被确定为一种新型的血管生成促进因子。本研究的目的是调查PDR后apelin与ERM之间的相关性。
方法
通过玻璃体切除术从12例PDR患者（年龄57±6岁；糖尿病病程16±7年）和12例特发性ERM患者（年龄68±5岁）获取ERM样本。对样本进行免疫组织化学和逆转录 - 聚合酶链反应（RT - PCR）处理。我们还分析了在玻璃体切除术前接受玻璃体内注射贝伐单抗（IVB）的PDR患者的样本。
结果
PDR的ERM中apelin的mRNA表达显著高于特发性ERM。相应地，免疫组织化学分析显示，在所有8例未接受IVB的PDR的ERM中apelin表达强烈，并且与胶质纤维酸性蛋白抗体（GFAP）、血小板内皮细胞黏附分子 - 1（CD31）、细胞角蛋白（CK）和血管内皮生长因子（VEGF）双标，但不与纤连蛋白双标。它们主要位于外膜。相比之下，IVB后的PDR的ERM和特发性ERM中apelin的表达较低。
结论
结果表明apelin参与了ERM的形成并促进了包括胶质细胞、内皮细胞和视网膜色素上皮细胞在内的外膜形成。贝伐单抗阻断了apelin的表达并减轻了胶质增生和血管生成。
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