Soluble Guanylate Cyclase α1–Deficient Mice: A Novel Murine Model for Primary Open Angle Glaucoma

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Soluble Guanylate Cyclase α1–Deficient Mice: A Novel Murine Model for Primary Open Angle Glaucoma

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Title: Soluble Guanylate Cyclase α1–Deficient Mice: A Novel Murine Model for Primary Open Angle Glaucoma
Author: Ko, Yu-Chieh; Hayton, Sarah R.; Jones, Alexander; Tainsh, Laurel T.; Ren, Ruiyi; Giani, Andrea; Clerté, Maeva; Abernathy, Emma; de Waard, Nadine; Turcotte, Raphael; Nathan, Daniel; Loomis, Stephanie J.; Gong, Haiyan; Brouckaert, Peter; Buys, Emmanuel; Alt, Clemens; Tainsh, Robert Edward Tillinghast; Oh, Dong-Jin; Malhotra, Rajeev; Arora, Pankaj; Yu, Binglan; Scherrer-Crosbie, Marielle; Kang, Jae Hee Hee; Lin, Charles P.; Rhee, Douglas J; Wiggs, Janey Lee; Gregory, Meredith S.; Pasquale, Louis; Bloch, Kenneth Daniel; Ksander, Bruce R.

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

Citation: Buys, Emmanuel, Yu-Chieh Ko, Clemens Alt, Sarah R. Hayton, Alexander Jones, Laurel T. Tainsh, Ruiyi Ren, et al. 2013. Soluble guanylate cyclase α1–deficient mice: A novel murine model for primary open angle glaucoma. PLoS ONE 8(3): e60156.
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Abstract: Primary open angle glaucoma (POAG) is a leading cause of blindness worldwide. The molecular signaling involved in the pathogenesis of POAG remains unknown. Here, we report that mice lacking the \(α_1\) subunit of the nitric oxide receptor soluble guanylate cyclase represent a novel and translatable animal model of POAG, characterized by thinning of the retinal nerve fiber layer and loss of optic nerve axons in the context of an open iridocorneal angle. The optic neuropathy associated with soluble guanylate cyclase \(α_1\)–deficiency was accompanied by modestly increased intraocular pressure and retinal vascular dysfunction. Moreover, data from a candidate gene association study suggests that a variant in the locus containing the genes encoding for the \(α_1\) and \(β_1\) subunits of soluble guanylate cyclase is associated with POAG in patients presenting with initial paracentral vision loss, a disease subtype thought to be associated with vascular dysregulation. These findings provide new insights into the pathogenesis and genetics of POAG and suggest new therapeutic strategies for POAG.
Published Version: doi:10.1371/journal.pone.0060156
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3603933/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:10622938
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