An immunohistochemical study of neuronal and glial cell reactions in retinae of rats with experimental glaucoma

Abstract

Glaucoma is a common disease seen in the eye clinic, but its associated pathological processes, especially the role of glial cells in glaucomatous retinae, are still under debate. The aim of the present work was to study the responses of astrocytes, Müller cells and microglia in retinae of rats with experimental glaucoma. Glaucoma was induced in adult male Wistar rats by cauterizing limbal-derived veins and the changes in glial fibrillary acidic protein (GFAP), OX42, OX18, OX6 and EDI expression were studied by immunohistochemical staining. Neuronal cell viability was studied by immunostaining with the neuronal nuclei (NeuN) antibody. In the experimental glaucomatous eyes, a significant drop in the number of NeuN-positive neurons was observed from 7 days postoperation and beyond in both the ganglion cell layer and inner nuclear layer. The expression of GFAP and OX42 was increased during the first 2 months after operation and reduced in rats at 3 and 4 months. OX6 and OX18 immunoreactivity was induced in some microglia of both glaucomatous and sham-operated control eyes. Possible mechanisms of the reaction of astrocytes, Müller cells and microglia in neuronal degeneration following glaucoma are discussed.

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

“…This is also in agreement with the common thought originated from in vivo experiments and clinical observations that glaucoma is a selective disease, which results in the degeneration of retinal neurons, specifically the RGCs and their axons. Obviously, despite preferential susceptibility of RGCs to primary and/or secondary degeneration in glaucoma, glial cells are relatively protected against glaucomatous injury, but rather they exhibit an activated phenotype, in vitro (Tezel et al, 2001a) and in vivo (Tanihara et al, 1997;Varela and Hernandez, 1997;Wang et al, 2002;Wang et al, 2000). This differential response of glial cells to tissue stress by activation persists during the chronic course of glaucomatous neurodegeneration .…”

Dynamic, in vivo, real-time detection of retinal oxidative status in a model of elevated intraocular pressure using a novel, reversibly responsive, profluorescent nitroxide probe

“…This was in stark contrast to the glial cell activation we and others see in injured retinas (Fig. 3) (Larsen and Osborne, 1996;Naskar et al, 2002;Wang et al, 2000). These data suggest that ME-TRN can be safely administered in the eye to monitor the dynamic processes of oxidative stress.…”

PAX6 Expression and Retinal Cell Death in a Transgenic Mouse Model for Acute Angle-Closure Glaucoma

“…Increased GFAP is commonly observed in degenerative retinal diseases, 35,36 whereas TIMP-1-encoding mRNA is elevated in microglia of glaucoma patients. 37 Activation of proinflammatory IL-1b might be involved in the etiology of glaucoma 35,38,39 and increased endothelin-2 expression occurs in human glaucoma during glial activation. 40 Late down-regulation of the caspase inhibitor XIAP and of Bcl-X L and Bcl-2 was observed in CLR SMaA mice on p82, similar to observations in degenerating retinas.…”