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Conference Paper: SIRT1 enhances endothelium-dependent relaxation through an eNOS-independent mechanism

TitleSIRT1 enhances endothelium-dependent relaxation through an eNOS-independent mechanism
Authors
KeywordsBiology
Issue Date2012
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 671.1 How to Cite?
AbstractSIRT1 is a class III NAD+-dependent deacetylase which involved in a wide range of cellular processes and possesses vascular protective effects. SIRT1 maintains vascular homeostasis by reducing endothelial activation, preventing endothelial senescence, and promoting endothelium-dependent relaxations of vascular smooth muscle. To elucidate the molecular mechanisms underlying the SIRT1-mediated vascular protection, an endothelium-specific SIRT1 transgenic mouse model was engineered. The vascular responsiveness of the thoracic aorta was determined using a Mulvany-Halpern wire myograph for the recording of isometric force. The results showed that selective over-expression of SIRT1 in endothelial cells significantly enhanced acetylcholine-evoked aortic relaxation in mice of different ages [8, 12, 16 and 20 weeks] and prevented high fat diet-induced endothelial dysfunction. The enhanced endothelium-dependent relaxation in the aorta of these SIRT1 transgenic mice persisted in the presence of L-NAME, an inhibitor of NO synthesis. Moreover, the eNOS activity was not significantly different from that in preparations of wild type mice. These findings suggest that an eNOS/NO independent mechanism is involved in the vascular regulation by SIRT1.
DescriptionSession - 671. Endothelial Mechanisms - Poster: no. 671.1
Persistent Identifierhttp://hdl.handle.net/10722/149246
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorXu, Cen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWang, Yen_US
dc.date.accessioned2012-06-22T06:32:05Z-
dc.date.available2012-06-22T06:32:05Z-
dc.date.issued2012en_US
dc.identifier.citationThe 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 671.1en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/149246-
dc.descriptionSession - 671. Endothelial Mechanisms - Poster: no. 671.1-
dc.description.abstractSIRT1 is a class III NAD+-dependent deacetylase which involved in a wide range of cellular processes and possesses vascular protective effects. SIRT1 maintains vascular homeostasis by reducing endothelial activation, preventing endothelial senescence, and promoting endothelium-dependent relaxations of vascular smooth muscle. To elucidate the molecular mechanisms underlying the SIRT1-mediated vascular protection, an endothelium-specific SIRT1 transgenic mouse model was engineered. The vascular responsiveness of the thoracic aorta was determined using a Mulvany-Halpern wire myograph for the recording of isometric force. The results showed that selective over-expression of SIRT1 in endothelial cells significantly enhanced acetylcholine-evoked aortic relaxation in mice of different ages [8, 12, 16 and 20 weeks] and prevented high fat diet-induced endothelial dysfunction. The enhanced endothelium-dependent relaxation in the aorta of these SIRT1 transgenic mice persisted in the presence of L-NAME, an inhibitor of NO synthesis. Moreover, the eNOS activity was not significantly different from that in preparations of wild type mice. These findings suggest that an eNOS/NO independent mechanism is involved in the vascular regulation by SIRT1.-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.subjectBiology-
dc.titleSIRT1 enhances endothelium-dependent relaxation through an eNOS-independent mechanismen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.emailWang, Y: yuwanghk@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros200067en_US
dc.identifier.volume26-
dc.identifier.issuemeeting abstract-
dc.publisher.placeUnited States-

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