Apoptotic retinal ganglion cell death in an autoimmune glaucoma model is accompanied by antibody depositions

Abstract

Glaucoma is characterized by death of retinal ganglion cells (RGC), but its cause is still unknown. We used an autoimmune glaucoma model to study (1) apoptosis, (2) antibody occurrence, and (3) gliosis by immunohistochemistry. Rats were immunized with optic nerve homogenate (ONA). At 8 days no significant apoptosis or difference in RGCs was noted, but ONA retinas had a significantly higher GFAP+ area (p = 0.02). At 14 days, significantly more TUNEL+ (p = 0.0002) and caspase 3+ (p = 0.004) were detected in ONA animals, but no difference in RGC density. Distinct IgM and IgG deposits (p = 0.04) were observed in ONA retinas. At 22 days, a significantly higher number of TUNEL+ cells (p = 0.0002), caspase 3+ cells (p = 0.0007), and concurrent a lower RGC density (p = 0.04) was noted in ONA animals. IgM and IgG deposits were observed in the ganglion cell layer of ONA retinas. The largest percentage of GFAP+ area in the ONA group was observed at 22 days (p = 0.02). This data suggest that immunization with ocular antigens leads to apoptotic retinal ganglion cell death. Based on the co-localization of antibody deposits and apoptotic cells, we conclude that antibodies are engaged in eliciting RGC apoptosis in this animal model. © 2013 Springer Science+Business Media New York.