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Article: Association of F11 receptor gene polymorphisms with central obesity and blood pressure
Title | Association of F11 receptor gene polymorphisms with central obesity and blood pressure |
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Authors | |
Keywords | Cell adhesion molecules F11 receptor Gene polymorphism Hypertension Obesity |
Issue Date | 2008 |
Publisher | Blackwell Publishing Ltd |
Citation | Journal Of Internal Medicine, 2008, v. 263 n. 3, p. 322-332 How to Cite? |
Abstract | Objectives. 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 Identifier | http://hdl.handle.net/10722/91573 |
ISSN | 2023 Impact Factor: 9.0 2023 SCImago Journal Rankings: 2.895 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ong, KL | en_HK |
dc.contributor.author | Leung, RYH | en_HK |
dc.contributor.author | Wong, LYF | en_HK |
dc.contributor.author | Cherny, SS | en_HK |
dc.contributor.author | Sham, PC | en_HK |
dc.contributor.author | Lam, TH | en_HK |
dc.contributor.author | Lam, KSL | en_HK |
dc.contributor.author | Cheung, BMY | en_HK |
dc.date.accessioned | 2010-09-17T10:21:35Z | - |
dc.date.available | 2010-09-17T10:21:35Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Journal Of Internal Medicine, 2008, v. 263 n. 3, p. 322-332 | en_HK |
dc.identifier.issn | 0954-6820 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/91573 | - |
dc.description.abstract | Objectives. 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.language | eng | en_HK |
dc.publisher | Blackwell Publishing Ltd | en_HK |
dc.relation.ispartof | Journal of Internal Medicine | en_HK |
dc.subject | Cell adhesion molecules | en_HK |
dc.subject | F11 receptor | en_HK |
dc.subject | Gene polymorphism | en_HK |
dc.subject | Hypertension | en_HK |
dc.subject | Obesity | en_HK |
dc.subject.mesh | Adult | en_HK |
dc.subject.mesh | Aged | en_HK |
dc.subject.mesh | Asian Continental Ancestry Group - genetics | en_HK |
dc.subject.mesh | Case-Control Studies | en_HK |
dc.subject.mesh | Cell Adhesion Molecules - genetics | en_HK |
dc.subject.mesh | Cohort Studies | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Hong Kong | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Hypertension - ethnology - genetics | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Middle Aged | en_HK |
dc.subject.mesh | Obesity - ethnology - genetics | en_HK |
dc.subject.mesh | Polymorphism, Single Nucleotide - genetics | en_HK |
dc.subject.mesh | Receptors, Cell Surface - genetics | en_HK |
dc.title | Association of F11 receptor gene polymorphisms with central obesity and blood pressure | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Cherny, SS: cherny@hku.hk | en_HK |
dc.identifier.email | Sham, PC: pcsham@hku.hk | en_HK |
dc.identifier.email | Lam, TH: hrmrlth@hkucc.hku.hk | en_HK |
dc.identifier.email | Lam, KSL: ksllam@hku.hk | en_HK |
dc.identifier.email | Cheung, BMY: mycheung@hku.hk | en_HK |
dc.identifier.authority | Cherny, SS=rp00232 | en_HK |
dc.identifier.authority | Sham, PC=rp00459 | en_HK |
dc.identifier.authority | Lam, TH=rp00326 | en_HK |
dc.identifier.authority | Lam, KSL=rp00343 | en_HK |
dc.identifier.authority | Cheung, BMY=rp01321 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1111/j.1365-2796.2007.01886.x | en_HK |
dc.identifier.pmid | 18067551 | en_HK |
dc.identifier.scopus | eid_2-s2.0-38849155809 | en_HK |
dc.identifier.hkuros | 142264 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-38849155809&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 263 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 322 | en_HK |
dc.identifier.epage | 332 | en_HK |
dc.identifier.eissn | 1365-2796 | - |
dc.identifier.isi | WOS:000252930400010 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Ong, KL=8340854000 | en_HK |
dc.identifier.scopusauthorid | Leung, RYH=7101876102 | en_HK |
dc.identifier.scopusauthorid | Wong, LYF=24476809800 | en_HK |
dc.identifier.scopusauthorid | Cherny, SS=7004670001 | en_HK |
dc.identifier.scopusauthorid | Sham, PC=34573429300 | en_HK |
dc.identifier.scopusauthorid | Lam, TH=7202522876 | en_HK |
dc.identifier.scopusauthorid | Lam, KSL=8082870600 | en_HK |
dc.identifier.scopusauthorid | Cheung, BMY=7103294806 | en_HK |
dc.identifier.citeulike | 2351260 | - |
dc.identifier.issnl | 0954-6820 | - |