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dc.contributor.authorMaguire, Janeten
dc.contributor.authorJones, Katie Len
dc.contributor.authorKuc, Rhoda Een
dc.contributor.authorClarke, Murrayen
dc.contributor.authorBennett, Martinen
dc.contributor.authorDavenport, Anthonyen
dc.date.accessioned2014-08-18T14:56:35Z
dc.date.available2014-08-18T14:56:35Z
dc.date.issued2013-12-09en
dc.identifier.citation(2014) Cardiovascular Research 101(3): 513-521en
dc.identifier.issn0008-6363
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/245724
dc.description.abstractAims The chemokine receptor CCR5 and its inflammatory ligands have been linked to atherosclerosis, an accelerated form of which occurs in saphenous vein graft disease. We investigated the function of vascular smooth muscle CCR5 in human coronary artery and saphenous vein, vascular tissues susceptible to atherosclerosis, and vasospasm. Methods and results CCR5 ligands were vasoconstrictors in saphenous vein and coronary artery. In vein, constrictor responses to CCL4 were completely blocked by CCR5 antagonists, including maraviroc. CCR5 antagonists prevented the development of a neointima after 14 days in cultured saphenous vein. CCR5 and its ligands were expressed in normal and diseased coronary artery and saphenous vein and localized to medial and intimal smooth muscle, endothelial, and inflammatory cells. [125I]-CCL4 bound to venous smooth muscle with KD = 1.15 ± 0.26 nmol/L and density of 22 ± 9 fmol mg−1 protein. Conclusions Our data support a potential role for CCR5 in vasoconstriction and neointimal formation in vitro and imply that CCR5 chemokines may contribute to vascular remodelling and augmented vascular tone in human coronary artery and vein graft disease. The repurposing of maraviroc for the treatment of cardiovascular disease warrants further investigation.
dc.languageEnglishen
dc.language.isoenen
dc.publisherOUP
dc.rightsAttribution 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/uk/*
dc.titleThe CCR5 chemokine receptor mediates vasoconstriction and stimulates intimal hyperplasia in human vessels in vitroen
dc.typeArticle
dc.description.versionThis is the final published version of the article. It was originally published by OUP in Cardiovascular Research here: http://cardiovascres.oxfordjournals.org/content/101/3/513.full.en
prism.endingPage521
prism.publicationDate2013en
prism.publicationNameCardiovascular Researchen
prism.startingPage513
prism.volume101en
dc.rioxxterms.funderBritish Heart Foundation Biotechnology and Biological Sciences Research Council
dc.rioxxterms.projectidPS/02/001 PG/05/127/19872
rioxxterms.versionofrecord10.1093/cvr/cvt333en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2013-12-09en
dc.contributor.orcidMaguire, Janet [0000-0002-9254-7040]
dc.contributor.orcidClarke, Murray [0000-0002-8215-8885]
dc.contributor.orcidBennett, Martin [0000-0002-2565-1825]
dc.contributor.orcidDavenport, Anthony [0000-0002-2096-3117]
dc.identifier.eissn1755-3245
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMRC (G1000847)
pubs.funder-project-idBritish Heart Foundation (RG/13/14/30314)
pubs.funder-project-idMRC (G0800784)
pubs.funder-project-idBritish Heart Foundation (FS/09/005/26845)
pubs.funder-project-idBritish Heart Foundation (FS/13/3/30038)


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Attribution 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution 2.0 UK: England & Wales