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

TitleRole of genetic variants in gene encoding lipocalin-2 in the development of elevated blood pressure
Authors
Issue Date2011
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk
Citation
The 16th Medical Research Conference (MRC 2011), The University of Hong Kong, Hong Kong, 22 January 2011. In Hong Kong Medical Journal, 2011, v. 17 n. 1 suppl. 1, p. 17, abstract no. 15 How to Cite?
AbstractIntroduction: Lipocalin-2 is recently recognised 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 in Hong Kong Chinese. Methods: 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 period of 6.4 years. Elevated blood pressure was defined as ≥130/85 mm Hg or taking anti-hypertensive medication. Results: There were only two haplotypes with frequency of >5%, namely AGATC (45.5%) and GGTCC (41.2%). Haplotype GGTCC was associated with elevated blood pressure at follow-up (OR=1.17 compared to haplotype AGATC, P=0.031 after adjusting for age and sex). Among 1381 subjects without elevated blood pressure at baseline, 321 subjects developed elevated blood pressure at follow-up. Haplotype GGTCC was associated with the development of elevated blood pressure at follow-up (OR=1.30 compared to haplotype AGATC, P=0.011 after adjusting for age, sex, systolic blood pressure, and follow-up duration; OR=1.44, P=0.0015 after further adjusting for other covariates). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher systolic blood pressure than non-carriers (119.7±16.4 mm Hg vs 117.9±17.3 mm Hg, P=0.043). Conclusion: Our findings suggest, for the first time, that genetic variants in LCN2 may affect blood pressure. Further studies on the role of lipocalin-2 in blood pressure regulation are warranted. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/140170
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorOng, KLen_US
dc.contributor.authorTso, AWKen_US
dc.contributor.authorCherny, SSen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorLam, THen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2011-09-23T06:08:05Z-
dc.date.available2011-09-23T06:08:05Z-
dc.date.issued2011en_US
dc.identifier.citationThe 16th Medical Research Conference (MRC 2011), The University of Hong Kong, Hong Kong, 22 January 2011. In Hong Kong Medical Journal, 2011, v. 17 n. 1 suppl. 1, p. 17, abstract no. 15en_US
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/140170-
dc.description.abstractIntroduction: Lipocalin-2 is recently recognised 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 in Hong Kong Chinese. Methods: 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 period of 6.4 years. Elevated blood pressure was defined as ≥130/85 mm Hg or taking anti-hypertensive medication. Results: There were only two haplotypes with frequency of >5%, namely AGATC (45.5%) and GGTCC (41.2%). Haplotype GGTCC was associated with elevated blood pressure at follow-up (OR=1.17 compared to haplotype AGATC, P=0.031 after adjusting for age and sex). Among 1381 subjects without elevated blood pressure at baseline, 321 subjects developed elevated blood pressure at follow-up. Haplotype GGTCC was associated with the development of elevated blood pressure at follow-up (OR=1.30 compared to haplotype AGATC, P=0.011 after adjusting for age, sex, systolic blood pressure, and follow-up duration; OR=1.44, P=0.0015 after further adjusting for other covariates). Among subjects not taking anti-hypertensive medication, carriers of the haplotype GGTCC had higher systolic blood pressure than non-carriers (119.7±16.4 mm Hg vs 117.9±17.3 mm Hg, P=0.043). Conclusion: Our findings suggest, for the first time, that genetic variants in LCN2 may affect blood pressure. Further studies on the role of lipocalin-2 in blood pressure regulation are warranted. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.-
dc.languageengen_US
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk-
dc.relation.ispartofHong Kong Medical Journalen_US
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleRole of genetic variants in gene encoding lipocalin-2 in the development of elevated blood pressureen_US
dc.typeConference_Paperen_US
dc.identifier.emailCheung, BMY: mycheung@hku.hken_US
dc.identifier.emailOng, KL: okl2000@hku.hken_US
dc.identifier.emailTso, AWK: awktso@hku.hken_US
dc.identifier.emailCherny, SS: cherny@hku.hken_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.authorityCheung, BMY=rp01321en_US
dc.identifier.authorityTso, AWK=rp00535en_US
dc.identifier.authorityCherny, SS=rp00232en_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.identifier.authorityLam, TH=rp00326en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros194406en_US
dc.identifier.volume17-
dc.identifier.issue1 suppl. 1-
dc.identifier.spage17, abstract no. 15-
dc.identifier.epage17, abstract no. 15-
dc.publisher.placeHong Kong-

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