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Conference Paper: Overexpression of SIRT1 in vascular endothelial cells prevents premature vascular and metabolic ageing in Per2 mutant mice

TitleOverexpression of SIRT1 in vascular endothelial cells prevents premature vascular and metabolic ageing in Per2 mutant mice
Authors
Issue Date2017
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
12th International Symposium on Resistance Arteries (ISRA 2017), Manchester, UK, 3-6 September 2017. Abstracts in Journal of Vascular Research, 2017, v. 54 n. Suppl. 2, p. 16 How to Cite?
AbstractBackground- SIRT1 is a longevity regulator implicated in the regulation of circadian rhythmicity, which facilitates the organisms to adapt to the external environment. PER2 is a member of the Period family of circadian regulators participating in the transcription-translational feedback loop of clock-control mechanisms. The present study was designed to evaluate the protective effects of SIRT1 in vascular endothelial cells on Per2 mutation-induced vascular and metabolic abnormalities. Methods and Results-Wild type (WT) and PER2 mutant (Per2Brdm2) mice without or with human SIRT1 selectively overexpressed in vascular endothelial cells (Per2Brdm2EC-SIRT1) were used in the present study. Mice were housed under 12-hour light/dark cycle and a controlled temperature conditions with free access to water and chow. Radiotelemetry transmitters were implanted for monitoring arterial blood pressures. Compared to WT mice, Per2Brdm2 mice exhibited a loss of dipping in the diurnal blood pressures at the age of eight-weeks and hypertension at the age of 24-weeks, both of which were prevented by SIRT1 overexpression in endothelial cells. The premature metabolic ageing phenotype caused by Per2 mutation, including decreased skeletal muscle mass and increased fat mass as well as altered insulin sensitivity, was also prevented by endothelial overexpression of SIRT1. Preliminary metabolomics analyses indicated that endothelial SIRT1 elicits the anti-vascular and metabolic ageing activities via modulating amino acid metabolism in skeletal muscle. Conclusion-Endothelial SIRT1 represents a promising target for anti-ageing therapies in both vascular and metabolic diseases.
DescriptionMonday Poster Session - Board 15
Persistent Identifierhttp://hdl.handle.net/10722/263111
ISSN
2017 Impact Factor: 2.029
2015 SCImago Journal Rankings: 1.119

 

DC FieldValueLanguage
dc.contributor.authorMan, AWC-
dc.contributor.authorLiu, EQ-
dc.contributor.authorGuo, Y-
dc.contributor.authorLuo, C-
dc.contributor.authorXu, AM-
dc.contributor.authorVanhoutte, PMGR-
dc.contributor.authorWang, Y-
dc.date.accessioned2018-10-12T02:09:00Z-
dc.date.available2018-10-12T02:09:00Z-
dc.date.issued2017-
dc.identifier.citation12th International Symposium on Resistance Arteries (ISRA 2017), Manchester, UK, 3-6 September 2017. Abstracts in Journal of Vascular Research, 2017, v. 54 n. Suppl. 2, p. 16-
dc.identifier.issn1018-1172-
dc.identifier.urihttp://hdl.handle.net/10722/263111-
dc.descriptionMonday Poster Session - Board 15-
dc.description.abstractBackground- SIRT1 is a longevity regulator implicated in the regulation of circadian rhythmicity, which facilitates the organisms to adapt to the external environment. PER2 is a member of the Period family of circadian regulators participating in the transcription-translational feedback loop of clock-control mechanisms. The present study was designed to evaluate the protective effects of SIRT1 in vascular endothelial cells on Per2 mutation-induced vascular and metabolic abnormalities. Methods and Results-Wild type (WT) and PER2 mutant (Per2Brdm2) mice without or with human SIRT1 selectively overexpressed in vascular endothelial cells (Per2Brdm2EC-SIRT1) were used in the present study. Mice were housed under 12-hour light/dark cycle and a controlled temperature conditions with free access to water and chow. Radiotelemetry transmitters were implanted for monitoring arterial blood pressures. Compared to WT mice, Per2Brdm2 mice exhibited a loss of dipping in the diurnal blood pressures at the age of eight-weeks and hypertension at the age of 24-weeks, both of which were prevented by SIRT1 overexpression in endothelial cells. The premature metabolic ageing phenotype caused by Per2 mutation, including decreased skeletal muscle mass and increased fat mass as well as altered insulin sensitivity, was also prevented by endothelial overexpression of SIRT1. Preliminary metabolomics analyses indicated that endothelial SIRT1 elicits the anti-vascular and metabolic ageing activities via modulating amino acid metabolism in skeletal muscle. Conclusion-Endothelial SIRT1 represents a promising target for anti-ageing therapies in both vascular and metabolic diseases.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR-
dc.relation.ispartofJournal of Vascular Research-
dc.relation.ispartof12th International Symposium on Resistance Arteries (ISRA 2017)-
dc.rightsJournal of Vascular Research. Copyright © S Karger AG.-
dc.rightsThe final, published version is available at https://doi.org/10.1159/000480116-
dc.titleOverexpression of SIRT1 in vascular endothelial cells prevents premature vascular and metabolic ageing in Per2 mutant mice-
dc.typeConference_Paper-
dc.identifier.emailMan, AWC: andyman@HKUCC-COM.hku.hk-
dc.identifier.emailLuo, C: cuiting@hku.hk-
dc.identifier.emailXu, AM: amxu@hkucc.hku.hk-
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityXu, AM=rp00485-
dc.identifier.authorityVanhoutte, PMGR=rp00238-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.volume54-
dc.identifier.issueSuppl. 2-
dc.identifier.spage16-
dc.identifier.epage16-
dc.publisher.placeSwitzerland-

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