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Abstract #53239 Published in IGR 15-1
Soluble guanylate cyclase α1-deficient mice: a novel murine model for primary open angle glaucoma
Buys ES; Ko YC; Alt C; Hayton SR; Jones A; Tainsh LT; Ren R; Giani A; Clerté M; Abernathy E; Tainsh RE; Oh DJ; Malhotra R; Arora P; de Waard N; Yu B; Turcotte R; Nathan D; Scherrer-Crosbie M; Loomis SJ; Kang JH; Lin CP; Gong H; Rhee DJ; BrouckaertPLoS ONE 2013; 8: e60156
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 α1 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 α1-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 α1 and β1 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.
Anesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America. Ebuys@partners.org
Full articleClassification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
