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M. C. Holman, R. Casson, A. Ebneter, J. P. Wood, G. Chidlow; Differential Expression of Inducible Heat Shock Proteins in the Rat Retina, Optic Nerve and Brain in Models of Neuronal Degeneration. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2105.
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© ARVO (1962-2015); The Authors (2016-present)
In the brain, induction of certain heat shock proteins (Hsps) in glial cells and neurons occurs in response to various noxious stimuli and may promote neuronal survival. Only limited, sometimes contradictory, information is available regarding the expression of inducible Hsps in the visual system. We studied the expression of four major inducible Hsps - Hsp27, -32 -70 and αB-crystallin - in the retina and optic nerve in various models of retinal ganglion cell (RGC) degeneration. For comparative purposes, expression of Hsps in the brain following injury was also determined.
Adult rats received one of the following insults: (1) Chronic ocular hypertension, induced by lasering the trabecular meshwork; (2) Chronic ischemia, achieved by permanent, bilateral occlusion of the common carotid arteries (2VO); (3) optic nerve transection (ONT); (4) excitotoxicity, induced by intravitreal injection of NMDA. (5) focal stroke, caused by permanent or temporary occlusion of the middle cerebral artery (MCAO). Rats were killed at various time points and tissues were processed for single and double-label immunohistochemistry, RT-PCR or Western blotting using standard methodologies.
In the brain, all four Hsps were induced following MCAO. Hsp27 and -32 were primarily expressed by astrocytes; Hsp70 by neurons. Chronic ocular hypertension, 2VO, ONT and NMDA-induced excitotoxicity all resulted in injury to, and subsequent death of, RGCs. All of these injuries caused Hsp27 expression by retinal and optic nerve astrocytes. Except for NMDA, each injury model also induced Hsp27 in surviving RGCs. Surprisingly, little change was observed in the expression of Hsp70 following any of these retinal injuries. αB-crystallin was induced in Müller cells, astrocytes and oligodendrocytes after RGC injury, while significant Hsp32 expression in the retina was only observed following 2VO.
The retina and brain respond differently with regard to induction of Hsps following injury. Hsp27 is strongly induced in both glial cells and RGCs after injury and may play a key role in limiting neuronal loss.
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