T Bek1. 1. Department of Ophthalmology, Arhus University Hospital, Arhus C, Denmark.
Abstract
PURPOSE: To study changes in retinal glial cell components in areas of vascular occlusion secondary to diabetic retinopathy. MATERIAL: 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). RESULTS: 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. CONCLUSIONS: 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.
PURPOSE: To study changes in retinal glial cell components in areas of vascular occlusion secondary to diabetic retinopathy. MATERIAL: The retina from ten eyes of six diabeticpatients 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). RESULTS: The study showed increased immunoreactivity to S-100 protein, corresponding to perivascularly located glial cells in the retina from diabeticpatients, 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. CONCLUSIONS: 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.