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DNA Methylation of the Aryl Hydrocarbon Receptor Repressor Associations With Cigarette Smoking and Subclinical Atherosclerosis
Author(s) -
Lindsay M. Reynolds,
Ma Wan,
Jingzhong Ding,
Jackson Taylor,
Kurt Lohman,
Dan Su,
Brian D. Bennett,
Devin K. Porter,
Ryan C. Gimple,
Gary S. Pittman,
Xuting Wang,
Timothy D. Howard,
David S. Siscovick,
Bruce M. Psaty,
Steven Shea,
Gregory L. Burke,
David R. Jacobs,
Stephen S. Rich,
James E. Hixson,
James H. Stein,
Hendrik G. Stunnenberg,
R. Graham Barr,
Joel D. Kaufman,
Wendy S. Post,
Ina Hoeschele,
David M. Herrington,
Douglas A. Bell,
Yongmei Liu
Publication year - 2015
Publication title -
circulation cardiovascular genetics
Language(s) - English
Resource type - Journals
eISSN - 1942-325X
pISSN - 1942-3268
DOI - 10.1161/circgenetics.115.001097
Subject(s) - dna methylation , aryl hydrocarbon receptor , methylation , cotinine , biomarker , aryl hydrocarbon receptor nuclear translocator , biology , medicine , chemistry , gene , endocrinology , gene expression , genetics , nicotine , transcription factor
Tobacco smoke contains numerous agonists of the aryl hydrocarbon receptor (AhR) pathway, and activation of the AhR pathway was shown to promote atherosclerosis in mice. Intriguingly, cigarette smoking is most strongly and robustly associated with DNA modifications to an AhR pathway gene, the AhR repressor (AHRR). We hypothesized that altered AHRR methylation in monocytes, a cell type sensitive to cigarette smoking and involved in atherogenesis, may be a part of the biological link between cigarette smoking and atherosclerosis.

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