Retinal glial cell responses and Fas/FasL activation in rats with chronic ocular hypertension
Brain Research, ISSN: 0006-8993, Vol: 1122, Issue: 1, Page: 209-221
2006
- 56Citations
- 29Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations56
- Citation Indexes56
- 56
- CrossRef43
- Captures29
- Readers29
- 29
Article Description
Responses in the retina post injury provoke glial reactions that are not completely understood. This study investigated the reaction of retinal glial cells and the expression and localization of the Fas and Fas-ligand (FasL) in rats with chronic ocular hypertension. Experimental glaucoma was induced in one eye of 60 Sprague–Dawley rats by cauterizing three episcleral vessels. It caused a moderate intraocular pressure (IOP) elevation and significant retinal ganglion cell (RGC) loss for at least 6 weeks in all animals. Immunohistochemical analysis revealed that the expression of GFAP and OX-42 increased in the injured retinae. Fas/FasL immunoreactivity was elevated in the microglia, and we also observed an incremental increase in Fas associated death domain (FADD) immunoreactivity in Müller glial cells and RGCs in the IOP-elevated retinae. The activation of glial cells and upregulation of Fas and FasL suggest that glial cells may contribute to Fas-mediated cell death in the neurodegeneration process of chronic ocular hypertensive retinal insult.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006899306027181; http://dx.doi.org/10.1016/j.brainres.2006.09.022; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33750740077&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/17045251; https://linkinghub.elsevier.com/retrieve/pii/S0006899306027181; https://dx.doi.org/10.1016/j.brainres.2006.09.022
Elsevier BV
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