Authors

Yun Ju Sung, Washington University School of Medicine in St. Louis
Lisa De Las Fuentes, Washington University School of Medicine in St. Louis
Thomas W. Winkler, Universität Regensburg
Daniel I. Chasman, Brigham and Women's Hospital
Amy R. Bentley, National Human Genome Research Institute (NHGRI)
Aldi T. Kraja, Washington University School of Medicine in St. Louis
Ioanna Ntalla, Barts and The London School of Medicine and Dentistry
Helen R. Warren, Barts and The London School of Medicine and Dentistry
Xiuqing Guo, Harbor-UCLA Medical Center
Karen Schwander, Washington University School of Medicine in St. Louis
Alisa K. Manning, Massachusetts General Hospital
Michael R. Brown, University of Texas Health Science Center at Houston
Hugues Aschard, Harvard T.H. Chan School of Public Health
Mary F. Feitosa, Washington University School of Medicine in St. Louis
Nora Franceschini, UNC Gillings School of Global Public Health
Yingchang Lu, Icahn School of Medicine at Mount Sinai
Ching Yu Cheng, Singapore Eye Research Institute
Xueling Sim, National University Health System
Dina Vojinovic, Erasmus MC
Jonathan Marten, MRC Human Genetics Unit
Solomon K. Musani, University of Mississippi School of Medicine
Tuomas O. Kilpeläinen, Novo Nordisk Foundation Center for Basic Metabolic Research
Melissa A. Richard, McGovern Medical School
Stella Aslibekyan, The University of Alabama at Birmingham
Traci M. Bartz, University of Washington School of Medicine
Rajkumar Dorajoo, A-Star, Genome Institute of Singapore
Changwei Li, University of Georgia
Yongmei Liu, Wake Forest University Health Sciences
Tuomo Rankinen, Pennington Biomedical Research Center
Albert Vernon Smith, Icelandic Heart Association
Salman M. Tajuddin, National Institute on Aging (NIA)
Bamidele O. Tayo, Loyola University Chicago
Wei Zhao, University of Michigan, Ann Arbor

Document Type

Article

Publication Date

8-1-2019

Abstract

Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene-smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene-smoking interaction analysis and 38 were newly identified (P < 5 × 10-8, false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.

Publication Source (Journal or Book title)

Human Molecular Genetics

First Page

2615

Last Page

2633

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