A Genome-wide study of blood pressure in African Americans accounting for gene-smoking interaction

• Type of Material: Article
• Authors: Jacquelyn Y. Taylor, Yale University; Karen Schwander, Washington University in St. Louis; Sharon L. R. Kardia, University of Michigan; Donna Arnett, University of Alabama, Birmingham; Jingjing Liang, Case Western Reserve University; Steven C. Hunt, University of Utah; D.C. Rao, Washington University in St. Louis; Yan Sun, Emory University
• Language: English
• Date: 2016-01-11
• Publisher: Nature Publishing Group
• Publication Version: Final Published Version
• Copyright Statement: © 2016, Macmillan Publishers Limited
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1038/srep18812
• Title of Journal or Parent Work: Scientific Reports
• ISSN: 2045-2322
• Volume: 6
• Start Page: 18812
• End Page: 18812
• Grant/Funding Information: Funding for this research was provided in part by the Robert Wood Johnson Foundation—Nurse Faculty Scholars Grant 64193, and National Institutes of Health cooperative agreements (U10) with NHLBI: HL54471, HL54472, HL54473, HL54495, HL54496, HL54497, HL54509, HL54515, 2 R01 HL55673-12, R01 HL107552, HL100185 and HL100245.
• Research Categories: Biology, Genetics; Health Sciences, Epidemiology

Abstract

Cigarette smoking has been shown to be a health hazard. In addition to being considered a negative lifestyle behavior, studies have shown that cigarette smoking has been linked to genetic underpinnings of hypertension. Because African Americans have the highest incidence and prevalence of hypertension, we examined the joint effect of genetics and cigarette smoking on health among this understudied population. The sample included African Americans from the genome wide association studies of HyperGEN (N = 1083, discovery sample) and GENOA (N = 1427, replication sample), both part of the FBPP. Results suggested that 2 SNPs located on chromosomes 14 (NEDD8; rs11158609; raw p = 9.80 × 10−9, genomic control-adjusted p = 2.09 × 10−7) and 17 (TTYH2; rs8078051; raw p = 6.28 × 10−8, genomic control-adjusted p = 9.65 × 10−7) were associated with SBP including the genetic interaction with cigarette smoking. These two SNPs were not associated with SBP in a main genetic effect only model. This study advances knowledge in the area of main and joint effects of genetics and cigarette smoking on hypertension among African Americans and offers a model to the reader for assessing these risks. More research is required to determine how these genes play a role in expression of hypertension.