血小板源性生长因子对增生性玻璃体视网膜病变增生膜形成的影响

目的 探讨血小板源性生长因子（platelet-derived growth factor,PDGF)在增生性玻璃体视网膜病变（proliferative vitreoretinopathy,PVR)增生膜形成中的作用及PVR增生膜中是否存在PDGF的分泌细胞与靶细胞。方法 选择PVR患者的手术标本,其中视网膜前膜（epiretinal membrane,ERM)和视网膜下膜（subretinal membrane,SRM)标本各7例。采用免疫电镜方法检测PDGF及其受体在ERM、SRM中的表达及其与ERM、SRM中两种主要细胞成分即视网膜色素上皮细胞和神经胶质细胞的关系。结果 PDGF－A基7例ERM中均表达阳性,在7例SRM中5例表达阳性,标记物主要位于ERM、SRM部分细胞的胞质中。PDGF－B在7例ERM中均表达阳性,在6例SRM中5例表达阳性,标记物主要位于SRM、SRM的部分细胞胞质中,尤其集中于细胞质内一些电子密度高的椭圆形或不规则形的分泌颗粒中。提示PDGF可由ERM、SRM局部细胞产生,其在ERM、SRM的发病中起重要作用。本实验中PDGF－A和PDGF－B分别与细胞角蛋白和神经胶质纤维酸性蛋白双标记,结果显示细胞角蛋白标记阳性的细胞即视网膜色素上皮细胞和神经胶质纤维酸性蛋白标记阳性细胞－神经胶质细胞中的PDGF－A、PDGF－B蛋白表达阳性,表明视网膜色素上皮细胞和神经胶质细胞是PDGF的分泌细胞。结论 PDGF可由PVR增生膜中的细胞产生,在PVR的发病中起重要作用。视网膜色素上皮细胞和神经胶质细胞是PDGF的分泌细胞,从而为自分泌物、旁分泌机制提供依据。

The effect of platelet-derived growth factor on the formation of proliferative vitreoretinopathy

OBJECTIVE: To study the actions of platelet-derived growth factor (PDGF) in proliferative membrane formation of proliferative vitreoretinopathy (PVR) and whether there is the existence of PDGF secreting cells and target cells. METHODS: Seven epiretinal membranes (ERM) and 7 subretinal membranes (SRM) obtained from eyes undergoing pars plana vitrectomy for retinal detachment complicated by PVR were studied. A panel of polyclonal antibodies against PDGF-A and -B ligands, PDGF-alpha and -beta receptors, cytokeratin the marker of retinal pigment epithelial (RPE) cell] and glial fibrillary acidic protein (the marker of glial cell) was used in immune electron microscopy to examine the expression of PDGF and PDGF receptors (PDGFR) in the membranes. The relationship of PDGF protein and the main cellular composition of ERM and SRM, retinal pigment epithelial and glial cells, was detected by using the double-labeling techniques of immune electron microscopy. RESULTS: Positive protein expression of PDGF-A located in the cytoplasm of some cells was detected in 7 ERMs and 5 of 7 SRMs. Positive protein expression of PDGF-B was detected in 7 ERMs and 5 of 6 SRMs, and it was located in the cytoplasm of some cells, especially in the secreting granules. RPE cells and glial cells were identified in ERMs and SRMs. PDGF receptors were not detected in the ERM and SRM in this research. Double-labeling of PDGF and cytokeratin showed that RPE cells were the secreting cells of PDGF. Similarly, double-labeling of PDGF and glial fibrillary acidic protein showed that glial cells were the secreting cells of PDGF. CONCLUSIONS: PDGF can be secreted by the cells of ERM and SRM. PDGF plays an important role in the pathogenesis of PVR. RPE and glial cells are the secreting cells of PDGF. The results indicate that PDGF affects cellular behavior by autocrine or paracrine mode in the formation of PVR.