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Alterations of Retinal Vasculature in Cystathionine-Beta-Synthase Mutant Mice, a Model of Hyperhomocysteinemia
Author(s) -
Amany Tawfik,
Mohamed AlShabrawey,
Penny Roon,
Srinivas Sonne,
Jason Covar,
Surapoon Matragoon,
Preethi S. Ganapathy,
Sally S. Atherton,
Azza B. ElRemessy,
Vadivel Ganapathy,
Sylvia B. Smith
Publication year - 2013
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.12-10536
Subject(s) - cystathionine beta synthase , retinal , occludin , glial fibrillary acidic protein , hyperhomocysteinemia , biology , homocysteine , retina , blood–retinal barrier , pathology , microbiology and biotechnology , endocrinology , tight junction , biochemistry , medicine , methionine , immunology , immunohistochemistry , diabetic retinopathy , amino acid , neuroscience , diabetes mellitus
Mice with moderate/severe hyperhomocysteinemia due to deficiency or absence of the cbs gene encoding cystathionine-beta-synthase (CBS) have marked retinal disruption, ganglion cell loss, optic nerve mitochondrial dysfunction, and ERG defects; those with mild hyperhomocysteinemia have delayed retinal morphological/functional phenotype. Excess homocysteine is a risk factor for cardiovascular diseases; however, it is not known whether excess homocysteine alters retinal vasculature.

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