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All rights reserved." } ], "http://purl.org/dc/elements/1.1/title" : [ { "@value" : "BEL Framework Large Corpus Document" } ], "http://purl.org/pav/authoredBy" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#_4" } ], "http://purl.org/pav/version" : [ { "@value" : "20131211" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#_3", "http://www.w3.org/ns/prov#value" : [ { "@value" : "OBJECTIVE: We tested the hypothesis that deficiency of cellular glutathione peroxidase (GPx-1) enhances susceptibility to endothelial dysfunction in mice with moderate hyperhomocysteinemia. METHODS AND RESULTS: Mice that were wild type (Gpx1+/+), heterozygous (Gpx1+/-), or homozygous (Gpx1-/-) for the mutated Gpx1 allele were fed a control diet or a high-methionine diet for 17 weeks. Plasma total homocysteine was elevated in mice on the high-methionine diet compared with mice on the control diet (23+/-3 versus 6+/-0.3 micromol/L, respectively; P<0.001) and was not influenced by Gpx1 genotype. In mice fed the control diet, maximal relaxation of the aorta in response to the endothelium-dependent dilator acetylcholine (10(-5) mol/L) was similar in Gpx1+/+, Gpx1+/-, and Gpx1-/- mice, but relaxation to lower concentrations of acetylcholine was selectively impaired in Gpx1-/- mice (P<0.05 versus Gpx1+/+ mice). In mice fed the high-methionine diet, relaxation to low and high concentrations of acetylcholine was impaired in Gpx1-/- mice (maximal relaxation 73+/-6% in Gpx1-/- mice versus 90+/-2% in Gpx1+/+ mice, P<0.05). No differences in vasorelaxation to nitroprusside or papaverine were observed between Gpx1+/+ and Gpx1-/- mice fed either diet. Dihydroethidium fluorescence, a marker of superoxide, was elevated in Gpx1-/- mice fed the high-methionine diet (P<0.05 versus Gpx1+/+ mice fed the control diet). CONCLUSIONS: These findings demonstrate that deficiency of GPx-1 exacerbates endothelial dysfunction in hyperhomocysteinemic mice and provides support for the hypothesis that hyperhomocysteinemia contributes to endothelial dysfunction through a peroxide-dependent oxidative mechanism." } ], "http://www.w3.org/ns/prov#wasQuotedFrom" : [ { "@id" : "http://www.ncbi.nlm.nih.gov/pubmed/12482825" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#_4", "http://www.w3.org/2000/01/rdf-schema#label" : [ { "@value" : "Selventa" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#assertion", "http://www.w3.org/ns/prov#hadPrimarySource" : [ { "@id" : "http://www.ncbi.nlm.nih.gov/pubmed/12482825" } ], "http://www.w3.org/ns/prov#wasDerivedFrom" : [ { "@id" : "http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel" }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#_3" } ] } ], "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#provenance" }, { "@graph" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA", "http://purl.org/dc/terms/created" : [ { "@type" : "http://www.w3.org/2001/XMLSchema#dateTime", "@value" : "2014-07-03T14:31:57.290+02:00" } ], "http://purl.org/pav/createdBy" : [ { "@id" : "http://orcid.org/0000-0001-6818-334X" }, { "@id" : "http://orcid.org/0000-0002-1267-0234" } ] } ], "@id" : "http://www.tkuhn.ch/bel2nanopub/RAzlb3wvmx_kF2h0qgpmkiWNJFvMlhEggtpuy3Mdx5nBA#pubinfo" } ]