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Article: Association of F11 receptor gene polymorphisms with central obesity and blood pressure

TitleAssociation of F11 receptor gene polymorphisms with central obesity and blood pressure
Authors
KeywordsCell adhesion molecules
F11 receptor
Gene polymorphism
Hypertension
Obesity
Issue Date2008
PublisherBlackwell Publishing Ltd
Citation
Journal Of Internal Medicine, 2008, v. 263 n. 3, p. 322-332 How to Cite?
AbstractObjectives. F11 receptor, also known as junctional adhesion molecule-1, in the autonomic nervous system is implicated in the development of hypertension in spontaneous hypertensive rats. We investigated the association of single nucleotide polymorphisms (SNPs) in the F11 receptor gene (F11R) with hypertension and central obesity in Hong Kong Chinese. Methods. Seven tagging SNPs were identified in the HapMap database. Genotyping was performed using Sequenom MassArray in 263 hypertensive subjects and 393 normotensive controls, of whom 263 matched the cases in age and sex. Results. When subjects on anti-hypertensive medication were excluded, rs790056 and rs2774276 were associated with lower systolic blood pressure (TT:124.8 ± 18.3 mmHg vs. TC + CC: 120.2 ± 15.5 mmHg, P = 0.004 and CC: 124.7 ± 18.5 mmHg vs. CG+GG: 120.5 ± 15.1 mmHg, P = 0.007 respectively). Comparing 213 subjects with central obesity with 213 controls matched for sex and age, rs2481084 and rs3737787 were associated with lower odds of central obesity (odds ratio = 0.516, P = 0.002 and odds ratio = 0.540, P = 0.005 respectively). All these associations remained significant after correction for multiple testing. Analysis of statistically similar SNPs suggested that the causative variants for systolic blood pressure were located in F11R, whilst those for central obesity could be due to causative variants in the transcription factor 1 gene immediately upstream. Conclusions. F11 receptor plays a role in blood pressure regulation, not only in rats but also in man. The link between F11 receptor and central obesity merits further investigation. © 2007 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/91573
ISSN
2014 Impact Factor: 6.063
2014 SCImago Journal Rankings: 2.315
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorOng, KLen_HK
dc.contributor.authorLeung, RYHen_HK
dc.contributor.authorWong, LYFen_HK
dc.contributor.authorCherny, SSen_HK
dc.contributor.authorSham, PCen_HK
dc.contributor.authorLam, THen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorCheung, BMYen_HK
dc.date.accessioned2010-09-17T10:21:35Z-
dc.date.available2010-09-17T10:21:35Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Internal Medicine, 2008, v. 263 n. 3, p. 322-332en_HK
dc.identifier.issn0954-6820en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91573-
dc.description.abstractObjectives. F11 receptor, also known as junctional adhesion molecule-1, in the autonomic nervous system is implicated in the development of hypertension in spontaneous hypertensive rats. We investigated the association of single nucleotide polymorphisms (SNPs) in the F11 receptor gene (F11R) with hypertension and central obesity in Hong Kong Chinese. Methods. Seven tagging SNPs were identified in the HapMap database. Genotyping was performed using Sequenom MassArray in 263 hypertensive subjects and 393 normotensive controls, of whom 263 matched the cases in age and sex. Results. When subjects on anti-hypertensive medication were excluded, rs790056 and rs2774276 were associated with lower systolic blood pressure (TT:124.8 ± 18.3 mmHg vs. TC + CC: 120.2 ± 15.5 mmHg, P = 0.004 and CC: 124.7 ± 18.5 mmHg vs. CG+GG: 120.5 ± 15.1 mmHg, P = 0.007 respectively). Comparing 213 subjects with central obesity with 213 controls matched for sex and age, rs2481084 and rs3737787 were associated with lower odds of central obesity (odds ratio = 0.516, P = 0.002 and odds ratio = 0.540, P = 0.005 respectively). All these associations remained significant after correction for multiple testing. Analysis of statistically similar SNPs suggested that the causative variants for systolic blood pressure were located in F11R, whilst those for central obesity could be due to causative variants in the transcription factor 1 gene immediately upstream. Conclusions. F11 receptor plays a role in blood pressure regulation, not only in rats but also in man. The link between F11 receptor and central obesity merits further investigation. © 2007 Blackwell Publishing Ltd.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltden_HK
dc.relation.ispartofJournal of Internal Medicineen_HK
dc.subjectCell adhesion moleculesen_HK
dc.subjectF11 receptoren_HK
dc.subjectGene polymorphismen_HK
dc.subjectHypertensionen_HK
dc.subjectObesityen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAsian Continental Ancestry Group - geneticsen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshCell Adhesion Molecules - geneticsen_HK
dc.subject.meshCohort Studiesen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshHypertension - ethnology - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshObesity - ethnology - geneticsen_HK
dc.subject.meshPolymorphism, Single Nucleotide - geneticsen_HK
dc.subject.meshReceptors, Cell Surface - geneticsen_HK
dc.titleAssociation of F11 receptor gene polymorphisms with central obesity and blood pressureen_HK
dc.typeArticleen_HK
dc.identifier.emailCherny, SS: cherny@hku.hken_HK
dc.identifier.emailSham, PC: pcsham@hku.hken_HK
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailCheung, BMY: mycheung@hku.hken_HK
dc.identifier.authorityCherny, SS=rp00232en_HK
dc.identifier.authoritySham, PC=rp00459en_HK
dc.identifier.authorityLam, TH=rp00326en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityCheung, BMY=rp01321en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2796.2007.01886.xen_HK
dc.identifier.pmid18067551en_HK
dc.identifier.scopuseid_2-s2.0-38849155809en_HK
dc.identifier.hkuros142264-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38849155809&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume263en_HK
dc.identifier.issue3en_HK
dc.identifier.spage322en_HK
dc.identifier.epage332en_HK
dc.identifier.eissn1365-2796-
dc.identifier.isiWOS:000252930400010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridOng, KL=8340854000en_HK
dc.identifier.scopusauthoridLeung, RYH=7101876102en_HK
dc.identifier.scopusauthoridWong, LYF=24476809800en_HK
dc.identifier.scopusauthoridCherny, SS=7004670001en_HK
dc.identifier.scopusauthoridSham, PC=34573429300en_HK
dc.identifier.scopusauthoridLam, TH=7202522876en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridCheung, BMY=7103294806en_HK
dc.identifier.citeulike2351260-

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