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Article: Persistence of the nitric oxide pathway in the aorta of hypercholesterolemic apolipoprotein-E-deficient mice

TitlePersistence of the nitric oxide pathway in the aorta of hypercholesterolemic apolipoprotein-E-deficient mice
Authors
Issue Date2003
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Journal Of Vascular Research, 2003, v. 40 n. 2, p. 87-96 How to Cite?
AbstractThe markers of the bioavailability of NO (endothelium-dependent relaxation to acetylcholine and cyclic GMP content) in the thoracic aorta of apolipoprotein-E-deficient (ApoE KO) mice, 20 weeks old with enriched cholesterol diet or 35 weeks old on regular chow, are not decreased, in contrast with other models of atherosclerosis. However, severe hypercholesterolemia, the presence of atherosclerotic lesions and increased NADPH oxidase activity have been reported as early as at 20 weeks of age. The present experiments were designed to test if an increased capacity of NO production in these mice explains this paradox. The expressions of the 3 isoforms of NO synthase (NOS) were compared in ApoE KO and C57Bl/6J mice using Western blot and localized by immunohistochemistry. No adaptive increase in the expression of NOS was detected in ApoE KO mice. NO bio-availability could also be preserved by upregulation of enzymes involved in redox status such as CuZn or Mn superoxide dismutase and catalase. However, these enzymes were less expressed in ApoE KO mice than in control mice. These results highlight that ApoE KO mice represent an atypical model of atherosclerosis. Copyright © 2003 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/171298
ISSN
2015 Impact Factor: 2.186
2015 SCImago Journal Rankings: 1.119
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorVilleneuve, Nen_US
dc.contributor.authorFortuno, Aen_US
dc.contributor.authorSauvage, Men_US
dc.contributor.authorFournier, Nen_US
dc.contributor.authorBreugnot, Cen_US
dc.contributor.authorJacquemin, Cen_US
dc.contributor.authorPetit, Cen_US
dc.contributor.authorGosgnach, Wen_US
dc.contributor.authorCarpentier, Nen_US
dc.contributor.authorVanhoutte, Pen_US
dc.contributor.authorVilaine, JPen_US
dc.date.accessioned2012-10-30T06:13:15Z-
dc.date.available2012-10-30T06:13:15Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Vascular Research, 2003, v. 40 n. 2, p. 87-96en_US
dc.identifier.issn1018-1172en_US
dc.identifier.urihttp://hdl.handle.net/10722/171298-
dc.description.abstractThe markers of the bioavailability of NO (endothelium-dependent relaxation to acetylcholine and cyclic GMP content) in the thoracic aorta of apolipoprotein-E-deficient (ApoE KO) mice, 20 weeks old with enriched cholesterol diet or 35 weeks old on regular chow, are not decreased, in contrast with other models of atherosclerosis. However, severe hypercholesterolemia, the presence of atherosclerotic lesions and increased NADPH oxidase activity have been reported as early as at 20 weeks of age. The present experiments were designed to test if an increased capacity of NO production in these mice explains this paradox. The expressions of the 3 isoforms of NO synthase (NOS) were compared in ApoE KO and C57Bl/6J mice using Western blot and localized by immunohistochemistry. No adaptive increase in the expression of NOS was detected in ApoE KO mice. NO bio-availability could also be preserved by upregulation of enzymes involved in redox status such as CuZn or Mn superoxide dismutase and catalase. However, these enzymes were less expressed in ApoE KO mice than in control mice. These results highlight that ApoE KO mice represent an atypical model of atherosclerosis. Copyright © 2003 S. Karger AG, Basel.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVRen_US
dc.relation.ispartofJournal of Vascular Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Metabolism - Pathologyen_US
dc.subject.meshApolipoproteins E - Geneticsen_US
dc.subject.meshArteriosclerosis - Metabolismen_US
dc.subject.meshCatalase - Metabolismen_US
dc.subject.meshCholesterol, Dietary - Pharmacologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEndothelium, Vascular - Enzymologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshHypercholesterolemia - Metabolism - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.subject.meshTyrosine - Analogs & Derivatives - Metabolismen_US
dc.titlePersistence of the nitric oxide pathway in the aorta of hypercholesterolemic apolipoprotein-E-deficient miceen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, P:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, P=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000070705en_US
dc.identifier.pmid12808344-
dc.identifier.scopuseid_2-s2.0-0038347442en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038347442&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume40en_US
dc.identifier.issue2en_US
dc.identifier.spage87en_US
dc.identifier.epage96en_US
dc.identifier.isiWOS:000183804800001-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridVilleneuve, N=7003458215en_US
dc.identifier.scopusauthoridFortuno, A=6701317544en_US
dc.identifier.scopusauthoridSauvage, M=7004518546en_US
dc.identifier.scopusauthoridFournier, N=7005974551en_US
dc.identifier.scopusauthoridBreugnot, C=6603192478en_US
dc.identifier.scopusauthoridJacquemin, C=7004759803en_US
dc.identifier.scopusauthoridPetit, C=23103771000en_US
dc.identifier.scopusauthoridGosgnach, W=6508025071en_US
dc.identifier.scopusauthoridCarpentier, N=7003555642en_US
dc.identifier.scopusauthoridVanhoutte, P=7202304247en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US

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