Opposing Roles For Membrane Bound and Soluble Fas Ligand in Glaucoma-Associated Retinal Ganglion Cell Death

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Opposing Roles For Membrane Bound and Soluble Fas Ligand in Glaucoma-Associated Retinal Ganglion Cell Death

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Title: Opposing Roles For Membrane Bound and Soluble Fas Ligand in Glaucoma-Associated Retinal Ganglion Cell Death
Author: Hackett, Caroline G.; Abernathy, Emma F.; Hohlbaum, Andreas M.; Moody, Krishna-sulayman L.; Hobson, Maura W.; Jones, Alexander; Karray, Saoussen; Giani, Andrea; John, Simon W. M.; Marshak-Rothstein, Ann; Gregory, Meredith S.; Lee, Karen S.; Saff, Rebecca Rose; Kolovou, Paraskevi-Evi; Chen, Dong Feng; Ksander, Bruce R.

Note: Order does not necessarily reflect citation order of authors.

Citation: Gregory, Meredith S., Caroline G. Hackett, Emma F. Abernathy, Karen S. Lee, Rebecca R. Saff, Andreas M. Hohlbaum, Krishna-sulayman L. Moody et al. 2011. Opposing roles for membrane bound and soluble Fas ligand in glaucoma-associated retinal ganglion cell death. PLoS ONE 6(3): e17659.
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Abstract: Glaucoma, the most frequent optic neuropathy, is a leading cause of blindness worldwide. Death of retinal ganglion cells (RGCs) occurs in all forms of glaucoma and accounts for the loss of vision, however the molecular mechanisms that cause RGC loss remain unclear. The pro-apoptotic molecule, Fas ligand, is a transmembrane protein that can be cleaved from the cell surface by metalloproteinases to release a soluble protein with antagonistic activity. Previous studies documented that constitutive ocular expression of FasL maintained immune privilege and prevented neoangeogenesis. We now show that FasL also plays a major role in retinal neurotoxicity. Importantly, in both TNF \(\alpha\) triggered RGC death and a spontaneous model of glaucoma, gene-targeted mice that express only full-length FasL exhibit accelerated RGC death. By contrast, FasL-deficiency, or administration of soluble FasL, protected RGCs from cell death. These data identify membrane-bound FasL as a critical effector molecule and potential therapeutic target in glaucoma.
Published Version: doi:10.1371/journal.pone.0017659
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3066205/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:8364924

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