Abstract
Abstract: :
Purpose: Elevated intraocular pressure is thought to be the most important cause of triggering and exacerbation of glaucomatous optic neuropathy and retinal ganglion cell death. The relationship between high intraocular pressure and these glaucomatous changes is yet undetermined. HSP-70, a member of heat-shock proteins, is induced during preconditioning stress and is known to be responsible for the cell survival from the various metabolic stresses such as ischemia and hyperthermia in neuronal tissues. In this study, we employed a rat glaucoma model and measure the alteration of the expression level of HSP-70 and HSC-70 in the retina by immunoblotting. Methods: The right eye of each rat was served as the glaucoma model. To make the glaucoma model, cauterization of three episcleral vessels was carried out. The left eye was served as a control. Thereafter, the whole retina was collected at 7 days, 1, 3 and 6 months after the treatment and the immunoblotting was conducted using the retinal homogenate to assess the alteration of the amount of HSP-70 and HSC-70. Results: In the cauterized eye, IOP elevation was maintained at least for 6 months, measured by a pneumatonometer, and no additional cauterization was necessary. Immunoblotting analysis showed increase in the density of the HSP-70 band from 7 days to 6 months after the treatment compared with the controls. On the other hand, the intensity of the band of HSC-70 did not show difference between the samples collected from the control and treated eyes throughout the experimental period. Conclusions: The elevated IOP induced HSP-70, not HSC-70 in the rat retina. The increased level of HSP-70 is maintained for up to 6 month under the chronically elevated IOP. Further investigation is needed to determine the role of the heat-shock proteins in the retinal tissue under the stressful condition.
Keywords: intraocular pressure • animal model • neuroprotection