Glial reactivity and impaired glutamate metabolism in short-term experimental diabetic retinopathy
Glial reactivity and impaired glutamate metabolism in short-term experimental diabetic retinopathy
复制标题
DOI:
10.2337/diabetes.47.5.815
复制
发表时间:
1998-05-01
期刊:
影响因子:
7.7
通讯作者:
Strother, JM
中科院分区:
文献类型:
--
作者:
Lieth, E;Barber, AJ;Strother, JM
The early pathophysiology of diabetic retinopathy and the involvement of neural and vascular malfunction are poorly understood. Glial cells provide structural and metabolic support for retinal neurons and blood vessels, and the cells become reactive in certain injury states, We therefore used the streptozotocin rat model of short-term diabetic retinopathy to study glial reactivity and other glial functions in the retina in the first months after onset of diabetes. With a two-site enzyme-linked immunosorbent assay, we measured the expression of the intermediate filament glial fibrillary acidic protein (GFAP). After 1 month, GFAP was largely unchanged, but within 3 months of the beginning of diabetes, it was markedly induced, by fivefold (P < 0.04). Immunohistochemical staining showed that the GFAP induction occurred both in astrocytes and in Muller cells. Consistent with a glial cell malfunction, the ability of retinas to convert glutamate into glutamine, assayed chromatographically with an isotopic method, was reduced in diabetic rats to 65% of controls (P