Department of Medicine, Division of Cardiovascular Medicine; Meyers Primary Care Institute; Department of Quantitative Health Sciences, Epidemiology Division
Cardiology | Cardiovascular Diseases | Cellular and Molecular Physiology | Genetics | Molecular Genetics
BACKGROUND: Atrial fibrillation (AF) involves substantial electrophysiological, structural and contractile remodeling. We hypothesize that characterizing gene expression might uncover important pathways related to AF.
METHODS AND RESULTS: We performed genome-wide whole blood transcriptomic profiling (Affymetrix Human Exon 1.0 ST Array) of 2446 participants (mean age 66 +/- 9 years, 55% women) from the Offspring cohort of Framingham Heart Study. The study included 177 participants with prevalent AF, 143 with incident AF during up to 7 years follow up, and 2126 participants with no AF. We identified seven genes statistically significantly up-regulated with prevalent AF. The most significant gene, PBX1 (P = 2.8 x 10(-7)), plays an important role in cardiovascular development. We integrated differential gene expression with gene-gene interaction information to identify several signaling pathways possibly involved in AF-related transcriptional regulation. We did not detect any statistically significant transcriptomic associations with incident AF.
CONCLUSION: We examined associations of gene expression with AF in a large community-based cohort. Our study revealed several genes and signaling pathways that are potentially involved in AF-related transcriptional regulation.
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Citation: PLoS One. 2014 May 7;9(5):e96794. doi: 10.1371/journal.pone.0096794. Link to article on publisher's site
Lin, Honghuang; Yin, Xiaoyan; Lunetta, Kathryn L.; Dupuis, Josee; McManus, David D.; Lubitz, Steven A.; Magnani, Jared W.; Joehanes, Roby; Munson, Peter J.; Larson, Martin G.; Levy, Daniel; Ellinor, Patrick T.; and Benjamin, Emelia J., "Whole blood gene expression and atrial fibrillation: the Framingham Heart Study" (2014). Meyers Primary Care Institute Publications and Presentations. 709.