Chen Y S, Hackett S F, Schoenfeld C L, Vinores M A, Vinores S A, Campochiaro P A
Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287-9277, USA.
Br J Ophthalmol. 1997 Oct;81(10):919-26. doi: 10.1136/bjo.81.10.919.
AIMS/BACKGROUND: Epiretinal membranes (ERMs) arise from a variety of causes or, in some cases, for unknown reasons. Once established, ERMs tend to progress, becoming more extensive and exerting increasing traction along the inner surface of the retina. One possible cause for their progression is the production of growth factors by cells within ERMs that may provide autocrine or paracrine stimulation. Platelet derived growth factor (PDGF) and its receptors have been localised to cells of ERMs and may play such a role. In this study, comparative data were sought for several other growth factors that have been implicated in ERM formation.
Immunohistochemical staining of ERMs was done for PDGF-A, PDGF-B, basic fibroblast growth factor (bFGF), three isoforms of transforming growth factor beta (TGF-beta), and vascular endothelial growth factor (VEGF) and its receptors, flt-1 and flk-1/KDR. Expression of flt-1 and flk-1/KDR was examined in cultured retinal pigmented epithelial (RPE) cells and retinal glia from postmortem eyes by immunohistochemistry and by reverse transcription coupled to polymerase chain reaction (RT-PCR).
Staining was most intense and most frequently observed for VEGF and PDGF-A, both in vascular and avascular ERMs. The majority of cells stained for VEGF in nine of 11 (81.8%) diabetic ERMs and in 14 of 24 (58.3%) proliferative vitreoretinopathy ERMs. The receptors for VEGF, flt-1, and flk-1/KDR were also identified on cells in ERMs and on cultured RPE cells. By RT-PCR, mRNA for flt-1 was identified in RPE cells and retinal glia, and mRNA for flk-1/KDR was identified in RPE cells.
These data show that VEGF and its receptors are localised to both vascular and avascular ERMs and suggest that VEGF, like PDGF-A, may be an autocrine and paracrine stimulator that may contribute to progression of vascular and avascular ERMs.
目的/背景：视网膜前膜（ERM）可由多种原因引起，或在某些情况下原因不明。一旦形成，ERM往往会进展，范围扩大，并在视网膜内表面产生越来越大的牵引力。其进展的一个可能原因是ERM内细胞产生生长因子，可能提供自分泌或旁分泌刺激。血小板衍生生长因子（PDGF）及其受体已定位到ERM细胞，可能发挥这样的作用。在本研究中，寻找了其他几种与ERM形成有关的生长因子的比较数据。
对ERM进行免疫组织化学染色，检测PDGF-A、PDGF-B、碱性成纤维细胞生长因子（bFGF）、转化生长因子β（TGF-β）的三种异构体、血管内皮生长因子（VEGF）及其受体flt-1和flk-1/KDR。通过免疫组织化学和逆转录聚合酶链反应（RT-PCR）检测培养的视网膜色素上皮（RPE）细胞和死后眼视网膜神经胶质细胞中flt-1和flk-1/KDR的表达。
在血管性和无血管性ERM中，VEGF和PDGF-A的染色最强且最常见。在11个糖尿病性ERM中的9个（81.8%）和24个增殖性玻璃体视网膜病变ERM中的14个（58.3%）中，大多数细胞VEGF染色阳性。ERM细胞和培养的RPE细胞上也鉴定出VEGF受体flt-1和flk-1/KDR。通过RT-PCR，在RPE细胞和视网膜神经胶质细胞中鉴定出flt-1的mRNA，在RPE细胞中鉴定出flk-1/KDR的mRNA。
这些数据表明，VEGF及其受体定位于血管性和无血管性ERM，提示VEGF与PDGF-A一样，可能是一种自分泌和旁分泌刺激物，可能促进血管性和无血管性ERM的进展。
