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G. Kalesnykas, J.A. Rantala, M. Niittykoski, R. Miettinen, K. Kaarniranta, A. Salminen, H. Uusitalo; Cellular Expression of Heat Shock Protein 25 in Retinal Ganglion Cells in Rat Glaucoma Model . Invest. Ophthalmol. Vis. Sci. 2006;47(13):425.
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The exact mechanism of retinal ganglion cells (RGCs) death in glaucoma is still unknown, although apoptosis was suggested to be the final common pathway. Prior to that, however, cells undergo a response to a variety of physiological stress factors which induce a rapid increase of heat shock proteins’ (HSPs) synthesis. HSPs are known to prevent protein aggregation and to facilitate refolding of misfolded proteins to ensure the survival of cells. In this study we aimed to investigate the temporal changes of HSP 25 kDa (HSP25) expression in RGCs in rat glaucoma model.
An elevated level of intraocular pressure was caused by laser photocoagulation of episcleral and limbal veins. A week later, the first group of rats (n=4) was sacrificed. The second laser treatment was performed for rats that were sacrificed 2 (n=4) and 3 (n=4) weeks after the first treatment. The RGCs were labelled using retrograde tracer Fluorogold (FG) 7 days before the animal sacrifice. The total number of RGCs in each retina was estimated using stereology. HSP25 positive cells were visualized using immunohistochemical methods.
The stereological counting revealed a significant 30.6% loss of FG–positive RGCs after three weeks in laser–treated eyes than that in controls. The cellular expression of HSP25 was observed only in laser–treated eyes. However, there were no significant differences in ganglion cells showing both retrograde labelling and HSP25 immunostaining between the different treatment groups.
Loss of RGCs in rat glaucoma model is accompanied with an increased expression of HSP25 in RGCs.
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