Androgen-Induced Progression of Arterial Calcification in Apolipoprotein E-Null Mice Is Uncoupled from Plaque Growth and Lipid Levels

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dc.contributor.author Mcrobb, Lucinda en_US
dc.contributor.author Handelsman, Dj en_US
dc.contributor.author Heather, Alison en_US
dc.contributor.editor en_US
dc.date.accessioned 2012-02-02T11:01:13Z
dc.date.available 2012-02-02T11:01:13Z
dc.date.issued 2009 en_US
dc.identifier 2010000994 en_US
dc.identifier.citation Mcrobb Lucinda, Handelsman Dj, and Heather Alison 2009, 'Androgen-Induced Progression of Arterial Calcification in Apolipoprotein E-Null Mice Is Uncoupled from Plaque Growth and Lipid Levels', Endocrine Soc, vol. 150, no. 2, pp. 841-848. en_US
dc.identifier.issn 0013-7227 en_US
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/15622
dc.description.abstract Arterial calcification has prognostic significance for cardiovascular outcomes, but its pathogenesis remains unclear. Calcification increases with age, but its prevalence in men suggests hormonal influence. In this study we analyzed the effect of exogenous androgens on calcification of advanced atherosclerotic lesions in the arterial tree of gonadally intact 34-wk-old male and female apolipoprotein E-null mice. Testosterone (T) increased calcification 3- to 4-fold (P < 0.05) in lesions of the innominate artery and aortic sinus. A nonaromatizable androgen, dihydrotestosterone, also increased lesion calcification in the innominate artery (2.4-fold, P < 0.05) but not the aortic sinus. The androgen-induced effects were independent of sex and occurred despite corresponding reductions in plaque area, the latter correlating inversely with increased serum high-density lipoprotein cholesterol levels. Androgen-induced calcification in the innominate artery was observed with up-regulation of local androgen receptor (AR) expression in response to T and dihydrotestosterone for both males and females but neither androgen influenced innominate artery estrogen receptor (ER)-a or -? expression in either sex. en_US
dc.language en_US
dc.publisher Endocrine Soc en_US
dc.relation.isbasedon http://dx.doi.org/10.1210/en.2008-0760 en_US
dc.title Androgen-Induced Progression of Arterial Calcification in Apolipoprotein E-Null Mice Is Uncoupled from Plaque Growth and Lipid Levels en_US
dc.parent Endocrinology en_US
dc.journal.volume 150 en_US
dc.journal.number 2 en_US
dc.publocation Chevy Chase, USA en_US
dc.identifier.startpage 841 en_US
dc.identifier.endpage 848 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 110300 en_US
dc.personcode 0000065911 en_US
dc.personcode 0000065904 en_US
dc.personcode 108123 en_US
dc.percentage 100 en_US
dc.classification.name Clinical Sciences en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity ISI:000262851200032 en_US
dc.description.keywords Estrogen-Receptor-Alpha; Cell-Adhesion Molecule-1; High-Density-Lipoprotein; Coronary Calcification; Gene-Expression; Cardiovascular-Disease; Postmenopausal Women; Replacement Therapy; Osteoblastic Cells; Gender-Differences en_US
dc.staffid 108123 en_US


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