Purchase this article with an account.
A. Zhou, C. Stowell, L. Wang, C. Piper, J. Lan, C. F. Burgoyne, G. A. Cioffi; A Comparison of Protein Expression Changes in Ischemic Retinas and Ischemic Brains. Invest. Ophthalmol. Vis. Sci. 2008;49(13):6110.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
A number of neuronal disorders in the brain and in the retina are attributed to ischemia-induced injury, including possibly glaucoma. To identify retina-specific mechanisms that may mediate the glaucomatous changes of the eye, we initiated a study to compare changes in protein expression levels in the brain and the retina after ischemic insults. In a quantitative mass spectrometry analysis of ischemic rat brains, over five hundreds proteins were identified. Among them, more than fifty proteins showed an increase in expression levels when compared with that of control brains, and several of them are known to be expressed also in the retina. The purpose of the work presented herein was to examine whether or not similar changes in expression levels of selected proteins occur in both ischemic brains and ischemic retinas, as a mean to identify retina-specific changes after ischemia.
In Sprague-Dawley rats, retinal ischemia was induced by elevating the intraocular pressure (IOP) to 110 mmHg for 60 minutes followed by 24-hour reperfusion. Retinal sections 12 µm inthickness were prepared at the end of reperfusion. Immunocytochemical analyses of selected proteins that showed a change after brain ischemia were performed.
Three selected proteins that were up-regulated in ischemic brains included: visinin-like protein 1 (VILIP-1, a calcium sensor protein), SLIT-2 (a molecular guidance cue in cellular migration), and semaphoring 6B (a protein involved in the nerve system development). A detectable presence of all three proteins in rat retina was evident by immunocytochemistry. In the ischemic retina, the level of SLIT-2 expression was higher than that in the control retina - a similar change as seen in the ischemic brain. VILIP-1 and Semaphorin 6B, on the other hand, showed a decrease in expression in the ischemic retina, in contrast to their changes in ischemic brains. The afore-described changes in the ischemic retina were most prominent in the RGC layer.
Ischemia-induced changes in protein expression appear to be protein-specific, tissue-dependent and may differ between the brain and the retina. A proteome-wide characterization of protein expression changes after retinal ischemia, and a comparison of such changes with that in the brain will help to determine the mechanisms that underlie the retina-specific response to ischemic stress in this tissue.
This PDF is available to Subscribers Only