Abstract
Purpose: :
Heat shock protein(HSP)70 has been known to have neuroprotective effect on the retina in vitro and in a rat glaucoma model. This study was to evaluate the inducible HSP70 expression after oxidative stress induced by glutathione depletion in the mouse retina.
Methods: :
Unregulated oxidative stress was induced by depletion of intracellular glutathione by systematic administration of buthionine sulphoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase. After 0, 1, 4 and 7 days of BSO administration, we examined expression of HSP by real time RT-PCR, immunoblot, and immunohistochemistry assay.
Results: :
From analysis of RT-PCR and immunoblot assay, expression of HSP70 was observed in control group(Day 0) and significantly decreased from 1day after BSO injection. Immunohistochemistry assay showed that expression of HSP70 was most prominent in photoreceptor layer among retinal layers and that depletion of glutathione decreased HSP70’s expression to a great extent in the ganglion cell layer.
Conclusions: :
HSP seems to be play important role in prevention of oxidative stress induced retinal cell injury. But, sudden depletion of glutathione may decrease the expression of HSP70 by down regulation. And ganglion cell layer is more vulnerable to oxidative stress than the other layers in retina.
Keywords: oxidation/oxidative or free radical damage • retina • ganglion cells