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Article: Role of genetic variants in the gene encoding lipocalin-2 in the development of elevated blood pressure

TitleRole of genetic variants in the gene encoding lipocalin-2 in the development of elevated blood pressure
Authors
KeywordsBlood pressure
Haplotype
Hypertension
Lipocalin-2
Single nucleotide polymorphism
Issue Date2011
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/10641963.asp
Citation
Clinical And Experimental Hypertension, 2011, v. 33 n. 7, p. 484-491 How to Cite?
AbstractLipocalin-2 is recently recognized as a biomarker of obesity and inflammation, which are both risk factors for hypertension. We therefore investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding lipocalin-2 (LCN2) with elevated blood pressure (BP) in Hong Kong Chinese. Five tagging SNPs were genotyped in 1936 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) with a median follow-up time of 6.4 years. Elevated BP was defined as ≥130/85 mmHg or taking anti-hypertensive medication. Haplotype GGTCC was associated with elevated BP at follow-up after adjusting for age and sex (odds ratio (OR) [95% confidence interval (CI)] = 1.17 [1.011.36], P = 0.031). Haplotype GGTCC was also an associated plasma CRP level 11.7% (95% CI: 2.625.9%) higher among subjects with elevated BP after adjusting for age and sex (P = 0.036). Among 1381 subjects without elevated BP at baseline, 321 subjects developed elevated BP at follow-up. Haplotype GGTCC was associated with the development of elevated BP at follow-up after adjusting for baseline age, sex, systolic blood pressure (SBP), and follow-up duration (OR [95% CI] = 1.30 [1.061.58], P = 0.011). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher SBP than noncarriers (119.7 ± 16.4 mmHg vs. 117.9 ± 17.3 mmHg, P = 0.043). Our findings suggest, for the first time, that genetic variants in LCN2 may affect BP. Further studies on the role of lipocalin-2 in BP regulation are warranted. © 2011 Informa Healthcare USA, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/129292
ISSN
2023 Impact Factor: 1.5
2023 SCImago Journal Rankings: 0.448
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilHKU7229/01M
HKU7626/07M
Sun Chieh Yeh Heart Foundation
Funding Information:

This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.

References

 

DC FieldValueLanguage
dc.contributor.authorOng, KLen_HK
dc.contributor.authorTso, AWKen_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.accessioned2010-12-23T08:34:47Z-
dc.date.available2010-12-23T08:34:47Z-
dc.date.issued2011en_HK
dc.identifier.citationClinical And Experimental Hypertension, 2011, v. 33 n. 7, p. 484-491en_HK
dc.identifier.issn1064-1963en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129292-
dc.description.abstractLipocalin-2 is recently recognized as a biomarker of obesity and inflammation, which are both risk factors for hypertension. We therefore investigated the association of common single nucleotide polymorphisms (SNPs) in the gene encoding lipocalin-2 (LCN2) with elevated blood pressure (BP) in Hong Kong Chinese. Five tagging SNPs were genotyped in 1936 subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) with a median follow-up time of 6.4 years. Elevated BP was defined as ≥130/85 mmHg or taking anti-hypertensive medication. Haplotype GGTCC was associated with elevated BP at follow-up after adjusting for age and sex (odds ratio (OR) [95% confidence interval (CI)] = 1.17 [1.011.36], P = 0.031). Haplotype GGTCC was also an associated plasma CRP level 11.7% (95% CI: 2.625.9%) higher among subjects with elevated BP after adjusting for age and sex (P = 0.036). Among 1381 subjects without elevated BP at baseline, 321 subjects developed elevated BP at follow-up. Haplotype GGTCC was associated with the development of elevated BP at follow-up after adjusting for baseline age, sex, systolic blood pressure (SBP), and follow-up duration (OR [95% CI] = 1.30 [1.061.58], P = 0.011). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher SBP than noncarriers (119.7 ± 16.4 mmHg vs. 117.9 ± 17.3 mmHg, P = 0.043). Our findings suggest, for the first time, that genetic variants in LCN2 may affect BP. Further studies on the role of lipocalin-2 in BP regulation are warranted. © 2011 Informa Healthcare USA, Inc.en_HK
dc.languageengen_US
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/10641963.aspen_HK
dc.relation.ispartofClinical and Experimental Hypertensionen_HK
dc.rightsClinical and Experimental Hypertension. Copyright © Informa Healthcare.-
dc.subjectBlood pressureen_HK
dc.subjectHaplotypeen_HK
dc.subjectHypertensionen_HK
dc.subjectLipocalin-2en_HK
dc.subjectSingle nucleotide polymorphismen_HK
dc.titleRole of genetic variants in the gene encoding lipocalin-2 in the development of elevated blood pressureen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1064-1963&volume=33&issue=7&spage=484&epage=491&date=2010&atitle=Role+of+genetic+variants+in+the+gene+encoding+lipocalin-2+in+the+development+of+elevated+blood+pressure-
dc.identifier.emailTso, AWK: awk.tso@gmail.comen_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.authorityTso, AWK=rp00535en_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.doi10.3109/10641963.2010.549276en_HK
dc.identifier.pmid21978028-
dc.identifier.scopuseid_2-s2.0-80053648031en_HK
dc.identifier.hkuros183458en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053648031&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue7en_HK
dc.identifier.spage484en_HK
dc.identifier.epage491en_HK
dc.identifier.isiWOS:000295618100008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridOng, KL=8340854000en_HK
dc.identifier.scopusauthoridTso, AWK=6701371436en_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.issnl1064-1963-

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