Whole Blood Gene Expression and Atrial Fibrillation: The Framingham Heart Study
Lunetta, Kathryn L.
McManus, David D.
Magnani, Jared W.
Munson, Peter J.
Larson, Martin G.
Benjamin, Emelia J.Note: Order does not necessarily reflect citation order of authors.
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CitationLin, H., X. Yin, K. L. Lunetta, J. Dupuis, D. D. McManus, S. A. Lubitz, J. W. Magnani, et al. 2014. “Whole Blood Gene Expression and Atrial Fibrillation: The Framingham Heart Study.” PLoS ONE 9 (5): e96794. doi:10.1371/journal.pone.0096794. http://dx.doi.org/10.1371/journal.pone.0096794.
AbstractBackground: 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 = 2.8×10−7), 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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