Bek T
Department of Ophthalmology, Arhus University Hospital, Arhus C, Denmark.
Acta Ophthalmol Scand. 1997 Aug;75(4):388-92. doi: 10.1111/j.1600-0420.1997.tb00395.x.
To study changes in retinal glial cell components in areas of vascular occlusion secondary to diabetic retinopathy.
The retina from ten eyes of six diabetic patients and from five eyes of five normal controls were studied for immunoreactivity to glial fibrillary acid protein and vimentin (glial cells), S-100 protein (perivascular glial cells), carbonic anhydrase isoenzyme II and CD-57 antigen (Müller cells), and CD-68 antigen (microglia).
The study showed increased immunoreactivity to S-100 protein, corresponding to perivascularly located glial cells in the retina from diabetic patients, except for areas of vascular occlusion where this immunoreactivity was absent. Furthermore, the material invading the lumen of former retinal vessels in areas of vascular occlusion showed immunoreactivity to CAH-II and CD-57, suggesting that this material represents ingrowth of retinal Müller cells.
The findings suggest that at least two types of changes in retinal glial cells are involved in the pathophysiology of diabetic retinopathy, i.e. 1) Reactive changes in the perivascular glial cells in the retina, and 2) Müller cell ingrowth into the former lumen of occluded retinal vessels.
研究糖尿病视网膜病变继发血管阻塞区域视网膜神经胶质细胞成分的变化。
对6例糖尿病患者的10只眼以及5例正常对照者的5只眼的视网膜进行研究,检测其对胶质纤维酸性蛋白和波形蛋白(神经胶质细胞)、S-100蛋白(血管周围神经胶质细胞)、碳酸酐酶同工酶II和CD-57抗原(米勒细胞)以及CD-68抗原(小胶质细胞)的免疫反应性。
研究显示,糖尿病患者视网膜中与血管周围神经胶质细胞相对应的S-100蛋白免疫反应性增加,但血管阻塞区域无此免疫反应性。此外,在血管阻塞区域侵入先前视网膜血管腔的物质对CAH-II和CD-57呈免疫反应性,提示该物质代表视网膜米勒细胞的向内生长。
研究结果表明,至少两种视网膜神经胶质细胞变化参与了糖尿病视网膜病变的病理生理过程,即1)视网膜血管周围神经胶质细胞的反应性变化,以及2)米勒细胞向内生长至阻塞视网膜血管的先前管腔。