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Estrogen is not neuroprotective in a rodent model of optic nerve stroke

PURPOSE: Nonarteritic anterior ischemic optic neuropathy (NAION) is an optic nerve (ON) infarct of retinal ganglion cell (RGC) axons, and the most common cause of ON-related sudden vision loss. Estrogen has been previously proposed as a neuroprotective treatment for central nervous system ischemia....

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Autores principales: Bernstein, Steven L., Mehrabyan, Zara, Guo, Yan, Moianie, Nima
Formato: Texto
Lenguaje:English
Publicado: Molecular Vision 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185481/
https://www.ncbi.nlm.nih.gov/pubmed/17982415
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author Bernstein, Steven L.
Mehrabyan, Zara
Guo, Yan
Moianie, Nima
author_facet Bernstein, Steven L.
Mehrabyan, Zara
Guo, Yan
Moianie, Nima
author_sort Bernstein, Steven L.
collection PubMed
description PURPOSE: Nonarteritic anterior ischemic optic neuropathy (NAION) is an optic nerve (ON) infarct of retinal ganglion cell (RGC) axons, and the most common cause of ON-related sudden vision loss. Estrogen has been previously proposed as a neuroprotective treatment for central nervous system ischemia. We evaluated estrogen's potential in post-ON infarct treatment to reduce neuronal loss following a model of NAION, rodent anterior ischemic optic neuropathy (rAION). METHODS: We used the rat rAION model, coupled to array and northern analyses, to evaluate estrogen-associated, early post-infarct retinal gene expression changes. rAION was induced in ovariectomized female rats, which were then treated with either estrogen or vehicle. Stereological analysis of post-rAION RGC numbers was performed, using retrograde RGC fill-labeling with fluorogold. RESULTS: rAION induces an early increase in estrogen expressed transcript-1 (EET-1), but EET-1 expression is not affected by systemic estrogen pretreatment. Post-rAION, there is no significant increase in RGC numbers in estrogen treated animals compared with vehicle-treated controls. Estrogen treatment following stroke does not increase preservation of ON structure, compared with vehicle controls. CONCLUSIONS: While the rAION-axonal stroke model is a useful adjunct for evaluating potential AION neuroprotective treatments, post-stroke estrogen administration does not appear neuroprotective in this form of central nervous system insult. Similarly, estrogen is likely to be ineffective in improving ON structural integrity following an ischemic infarct.
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spelling pubmed-21854812008-02-13 Estrogen is not neuroprotective in a rodent model of optic nerve stroke Bernstein, Steven L. Mehrabyan, Zara Guo, Yan Moianie, Nima Mol Vis Research Article PURPOSE: Nonarteritic anterior ischemic optic neuropathy (NAION) is an optic nerve (ON) infarct of retinal ganglion cell (RGC) axons, and the most common cause of ON-related sudden vision loss. Estrogen has been previously proposed as a neuroprotective treatment for central nervous system ischemia. We evaluated estrogen's potential in post-ON infarct treatment to reduce neuronal loss following a model of NAION, rodent anterior ischemic optic neuropathy (rAION). METHODS: We used the rat rAION model, coupled to array and northern analyses, to evaluate estrogen-associated, early post-infarct retinal gene expression changes. rAION was induced in ovariectomized female rats, which were then treated with either estrogen or vehicle. Stereological analysis of post-rAION RGC numbers was performed, using retrograde RGC fill-labeling with fluorogold. RESULTS: rAION induces an early increase in estrogen expressed transcript-1 (EET-1), but EET-1 expression is not affected by systemic estrogen pretreatment. Post-rAION, there is no significant increase in RGC numbers in estrogen treated animals compared with vehicle-treated controls. Estrogen treatment following stroke does not increase preservation of ON structure, compared with vehicle controls. CONCLUSIONS: While the rAION-axonal stroke model is a useful adjunct for evaluating potential AION neuroprotective treatments, post-stroke estrogen administration does not appear neuroprotective in this form of central nervous system insult. Similarly, estrogen is likely to be ineffective in improving ON structural integrity following an ischemic infarct. Molecular Vision 2007-10-09 /pmc/articles/PMC2185481/ /pubmed/17982415 Text en Copyright © 2008 Molecular Vision. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Bernstein, Steven L.
Mehrabyan, Zara
Guo, Yan
Moianie, Nima
Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title_full Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title_fullStr Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title_full_unstemmed Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title_short Estrogen is not neuroprotective in a rodent model of optic nerve stroke
title_sort estrogen is not neuroprotective in a rodent model of optic nerve stroke
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185481/
https://www.ncbi.nlm.nih.gov/pubmed/17982415
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