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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom