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X. Chen, J. Bao, Y. Liu, N. Li, M. Li, R. Pan, D. Liu; Protective Effects of the Inducible Heat Shock Protein 72 on Retinal Ganglion Cells in a Rat Glaucoma Model . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3919.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether the heat shock protein (HSP) 72 can be induced in retinal ganglion cells (RGCs) by intraperitoneal zinc sulfate administration, and whether the induced HSP72 can increase survival of RGCs in experimental rat glaucoma.
Randomly, zinc sulfate (24.6mg/kg) or physiological saline was injected into 24 Wistar rats intraperitoneally once a week. Intraocular pressure (IOP) was elevated unilaterally by repeated trabecular argon laser photocoagulation after the second time of zinc or saline injection, the opposite eye served as a control. Subsequent to 7 weeks of IOP elevation, eyes were enucleated and RGC density was estimated by counting fluorescent dye–labeled cells in the flatmount of the retina. RGC apoptosis was evaluated by TdT–mediated biotin–dUTP nick end labeling (TUNEL). Immunohistochemical staining for Hsp72 was also performed.
The mean IOPs were 27.15±6.02 mmHg and 12.30±3.48mmHg in the laser treated eyes and in the control eyes, respectively (p<0.001). HSP72 was detected only in the eyes of the rats with zinc sulfate injection. The average density of RGC in the hypertensive eyes was 2,548±812/mm2 in the rats treated with zinc, and 2,003±690/mm2 in the rats treated with saline (p<0.001). The average density of RGC in the normotensive eyes was 2,573±765/mm2 in the rats treated with zinc, and 2,575±724/mm2 in the rats treated with saline (p>0.5). In the hypertensive eyes, the numbers of apoptotic RGC were 1.08±0.55/mm2 and 2.83±1.07/mm2 in the rats treated with zinc and with saline, respectively (p<0.01).
Endogenous HSP72 could be induced in RGCs by zinc sulfate administration systematically, and the induced HSP72 might increase the survival of RGCs in experimental rat glaucoma. Our results suggested that HSP72 induction could be a potential therapeutic approach for neuroprotection in glaucoma therapy.
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