Article: Plasma levels of fibrinogen and C-reactive protein are related to interleukin-6 gene -572C>G polymorphism in subjects with and without hypertension

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TitlePlasma levels of fibrinogen and C-reactive protein are related to interleukin-6 gene -572C>G polymorphism in subjects with and without hypertension
AuthorsWong, LYF1
Leung, RYH1
Ong, KL1
Cheung, BMY1
KeywordsChemicals And Cas Registry Numbers
Issue Date2007
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jhh
CitationJournal Of Human Hypertension, 2007, v. 21 n. 11, p. 875-882 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.jhh.1002233
AbstractHypertension is an important risk factor for cardiovascular diseases. There is increasing evidence suggesting that inflammation is involved in the development of hypertension. Interleukin-6 (IL-6) is an important mediator of inflammatory response and the major regulator of hepatic production of acute phase proteins, such as fibrinogen and C-reactive protein (CRP), which have been associated with hypertension and cardiovascular diseases. Therefore, we studied the association of single nucleotide polymorphism (SNP) in the IL-6 gene (IL6) promoter with plasma levels of fibrinogen, CRP and hypertension. Five hundred and two Hong Kong Chinese subjects (282 normotensives and 220 hypertensives) were recruited. IL-6 gene promoter was examined for polymorphism and the study subjects were genotyped for any SNP identified. The IL6 -572C>G polymorphism (rs1800796) was found with a frequency of 0.23 for the minor G allele. Subjects with the -572G allele had significantly higher plasma fibrinogen (3.06 ± 0.57 vs 2.83 ± 0.60, P = 0.002) and CRP (interquartile range 0.33-1.56 vs 0.12-0.93, P = 0.003) levels than those without. The -572C>G polymorphism was found to be an independent predictor of fibrinogen and CRP levels after adjusting for confounding factors. Plasma concentrations of fibrinogen and CRP correlated with systolic blood pressure. However, the -572C>G genotype frequencies did not differ between hypertensive and normotensive subjects, and there was no association between -572C>G polymorphism and blood pressure. Our results provide evidence that there is a clear genetic influence of IL6 -572C>G polymorphism on plasma levels of fibrinogen and CRP, but this polymorphism does not lead to elevated blood pressure.
ISSN0950-9240
2011 Impact Factor: 2.802
2011 SCImago Journal Rankings: 0.206
DOIhttp://dx.doi.org/10.1038/sj.jhh.1002233
ISI Accession Number IDWOS:000250225800005
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorWong, LYF
dc.contributor.authorLeung, RYH
dc.contributor.authorOng, KL
dc.contributor.authorCheung, BMY
dc.date.accessioned2010-09-17T10:23:38Z
dc.date.available2010-09-17T10:23:38Z
dc.date.issued2007
dc.description.abstractHypertension is an important risk factor for cardiovascular diseases. There is increasing evidence suggesting that inflammation is involved in the development of hypertension. Interleukin-6 (IL-6) is an important mediator of inflammatory response and the major regulator of hepatic production of acute phase proteins, such as fibrinogen and C-reactive protein (CRP), which have been associated with hypertension and cardiovascular diseases. Therefore, we studied the association of single nucleotide polymorphism (SNP) in the IL-6 gene (IL6) promoter with plasma levels of fibrinogen, CRP and hypertension. Five hundred and two Hong Kong Chinese subjects (282 normotensives and 220 hypertensives) were recruited. IL-6 gene promoter was examined for polymorphism and the study subjects were genotyped for any SNP identified. The IL6 -572C>G polymorphism (rs1800796) was found with a frequency of 0.23 for the minor G allele. Subjects with the -572G allele had significantly higher plasma fibrinogen (3.06 ± 0.57 vs 2.83 ± 0.60, P = 0.002) and CRP (interquartile range 0.33-1.56 vs 0.12-0.93, P = 0.003) levels than those without. The -572C>G polymorphism was found to be an independent predictor of fibrinogen and CRP levels after adjusting for confounding factors. Plasma concentrations of fibrinogen and CRP correlated with systolic blood pressure. However, the -572C>G genotype frequencies did not differ between hypertensive and normotensive subjects, and there was no association between -572C>G polymorphism and blood pressure. Our results provide evidence that there is a clear genetic influence of IL6 -572C>G polymorphism on plasma levels of fibrinogen and CRP, but this polymorphism does not lead to elevated blood pressure.
dc.description.naturelink_to_subscribed_fulltext
dc.identifier.citationJournal Of Human Hypertension, 2007, v. 21 n. 11, p. 875-882 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.jhh.1002233
dc.identifier.citeulike1302636
dc.identifier.doihttp://dx.doi.org/10.1038/sj.jhh.1002233
dc.identifier.eissn1476-5527
dc.identifier.epage882
dc.identifier.hkuros180162
dc.identifier.isiWOS:000250225800005
dc.identifier.issn0950-9240
2011 Impact Factor: 2.802
2011 SCImago Journal Rankings: 0.206
dc.identifier.issue11
dc.identifier.pmid17508011
dc.identifier.scopuseid_2-s2.0-34848822828
dc.identifier.spage875
dc.identifier.urihttp://hdl.handle.net/10722/91700
dc.identifier.volume21
dc.languageeng
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jhh
dc.publisher.placeUnited Kingdom
dc.relation.ispartofJournal of Human Hypertension
dc.relation.referencesReferences in Scopus
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshBlood Pressure
dc.subject.meshC-Reactive Protein - analysis - physiology
dc.subject.meshFemale
dc.subject.meshFibrinogen - analysis
dc.subject.meshGenotype
dc.subject.meshHumans
dc.subject.meshHypertension - blood - genetics
dc.subject.meshInterleukin-6 - genetics
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshPolymorphism, Single Nucleotide
dc.subject.meshPromoter Regions, Genetic
dc.subjectChemicals And Cas Registry Numbers
dc.titlePlasma levels of fibrinogen and C-reactive protein are related to interleukin-6 gene -572C>G polymorphism in subjects with and without hypertension
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong