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

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Show simple item record Mcrobb, L Handelsman, D Heather, AK 2012-02-02T11:01:13Z 2009-01
dc.identifier.citation Endocrinology, 2009, 150 (2), pp. 841 - 848
dc.identifier.issn 0013-7227
dc.identifier.other C1UNSUBMIT en_US
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 -ß expression in either sex.
dc.publisher Endocrine Soc
dc.relation.isbasedon 10.1210/en.2008-0760
dc.title Androgen-Induced Progression of Arterial Calcification in Apolipoprotein E-Null Mice Is Uncoupled from Plaque Growth and Lipid Levels
dc.type Journal Article
dc.parent Endocrinology
dc.journal.volume 2
dc.journal.volume 150
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 SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 1103 Clinical Sciences
dc.personcode 108123
dc.percentage 100 en_US Clinical Sciences en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US 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.description.keywords Estrogen-Receptor-Alpha
dc.description.keywords Cell-Adhesion Molecule-1
dc.description.keywords High-Density-Lipoprotein
dc.description.keywords Coronary Calcification
dc.description.keywords Gene-Expression
dc.description.keywords Cardiovascular-Disease
dc.description.keywords Postmenopausal Women
dc.description.keywords Replacement Therapy
dc.description.keywords Osteoblastic Cells
dc.description.keywords Gender-Differences
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Faculty of Science/School of Medical and Molecular Sciences
utslib.copyright.status Closed Access 2015-04-15 12:17:09.805752+10
utslib.collection.history Closed (ID: 3)
utslib.collection.history School of Medical and Molecular Sciences (ID: 341)

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