Authors

Tianxiao Huan, Framingham Heart Study
Tõnu Esko, Tartu Ülikooli Genoomika Instituut
Marjolein J. Peters, Erasmus MC
Luke C. Pilling, University of Exeter
Katharina Schramm, Helmholtz Center Munich German Research Center for Environmental Health
Claudia Schurmann, Universitätsmedizin Greifswald
Brian H. Chen, Framingham Heart Study
Chunyu Liu, Framingham Heart Study
Roby Joehanes, Framingham Heart Study
Andrew D. Johnson, Framingham Heart Study
Chen Yao, Framingham Heart Study
Sai xia Ying, NIH Center for Information Technology (CIT)
Paul Courchesne, Framingham Heart Study
Lili Milani, Tartu Ülikooli Genoomika Instituut
Nalini Raghavachari, National Institute on Aging (NIA)
Richard Wang, National Heart, Lung, and Blood Institute (NHLBI)
Poching Liu, National Heart, Lung, and Blood Institute (NHLBI)
Eva Reinmaa, Tartu Ülikooli Genoomika Instituut
Abbas Dehghan, Netherlands Genomics Initiative
Albert Hofman, Netherlands Genomics Initiative
André G. Uitterlinden, Erasmus MC
Dena G. Hernandez, National Institute on Aging (NIA)
Stefania Bandinelli, Azienda Sanitaria di Firenze
Andrew Singleton, National Institute on Aging (NIA)
David Melzer, University of Exeter
Andres Metspalu, Tartu Ülikooli Genoomika Instituut
Maren Carstensen, Heinrich-Heine-Universität Düsseldorf
Harald Grallert, Helmholtz Center Munich German Research Center for Environmental Health
Christian Herder, Heinrich-Heine-Universität Düsseldorf
Thomas Meitinger, Helmholtz Center Munich German Research Center for Environmental Health
Annette Peters, Helmholtz Center Munich German Research Center for Environmental Health
Michael Roden, Heinrich-Heine-Universität Düsseldorf
Melanie Waldenberger, Helmholtz Center Munich German Research Center for Environmental Health

Document Type

Article

Publication Date

3-18-2015

Abstract

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%–9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension.

Publication Source (Journal or Book title)

PLoS Genetics

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