Differential expression of heat shock protein mRNAs under in vivo glutathione depletion in the mouse retina

摘要: Heat shock proteins (HSPs) are highly conserved playing a protective role under deleterious conditions caused by wide variety of pathophysiological, including environmental stresses. Glutathione (GSH) is known to play critical in the cellular defense against unregulated oxidative stress mammalian cells neurons. We previously demonstrated that GSH depletion induced cell death retina, but mechanism(s) protection were not clear. Unregulated was intracellular systematic administration buthionine sulphoximine (BSO), an inhibitor gamma-glutamylcysteine synthetase. After 0, 1, 4 and 7 days BSO administration, we examined expression both large small HSP mRNAs (hsp90alpha, hsp90beta, hsp70, hsp60 hsp25) oxidative-stressed mouse retina. Of HSPs, only hsp70 significantly decreased from 1 day after injection, whereas other hsps changed on 1. Expression days, hsp90 administration. Different HSP, hsp25 increased its great extent Taken together, our results show could induce differential which, turn, may distinct roles defense. Targeting therefore, provide novel tools for treatment retinal degenerative diseases such as glaucoma, retinopathy or age-related macular degeneration.