Abstract
Abstract: :
Purpose: To study the activation of JNK in the retina of a rat glaucoma model. Methods: Adult male Wistar albino rats, 45–50 day–old, were given unilateral intravitreal injections of India ink, and trabecular laser photocoagulation was delivered 5 days after injection while the contralateral eye was used as a control. Intraocular pressure (IOP) was monitored. Eyes were enucleated at 1, 3, 7, 14, and 35 days after photocoagulation. The eyes were bisected and processed for immunohistochemistry with specific antibody against phosphorylated (activated) JNK proteins and TdT–mediated biotin–dUTP nick end labeling (TUNEL). A minimum of 6 eyes was examined for each group. Results: IOP increased by 66% compared to controls and was sustained (P=0.0001; n=41). Three days after IOP elevation, there was moderately increased immunoreactivity of phosphorylated JNK in scattered retinal ganglion cell (RGC) layer cells. More intense immunoreactivity was noted in cells at the RGC layer at 7 and 14 days after IOP elevation. At 35 days, there were some cells with mildly increased immunoreactivity in the RGC layer. After 7 days of IOP elevation, the number of TUNEL positive cells in the RGC layer was 1.2±0.3 per retinal section. The majority of TUNEL positive nuclei were double–labeled with mild immunoreactivity for phoshorylated JNK while some TUNEL positive nuclei were labeled with intense immunoreactivity of phosphorylated JNK. Conclusions: Activation of JNK pathway may play a role in RGC death in experimental glaucoma.
Keywords: ganglion cells • cell death/apoptosis • signal transduction