Journal
HUMAN MOLECULAR GENETICS
Volume 18, Issue 12, Pages 2288-2296Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddp135
Keywords
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Funding
- Wellcome Trust International Senior Research Fellowship [070191/Z/03/Z]
- Alexander-von-Humboldt Foundation partnership [V-Fokoop-EST/1051368, V-Fokoop-1113183]
- Estonian Ministry of Education and Science core [0182721s06]
- HHMI International Scholarship [55005617]
- Estonian Science Foundation [ETF7491]
- Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Neuherberg, Germany
- German Federal Ministry of Education and Research (BMBF)
- German National Genome Research Network (NGFN)
- Medical Research Council of Great Britain [G9521010D]
- British Heart Foundation [PG02/128]
- Wellcome Trust [070191/Z/03/Z, 076113/B/04/Z]
- Barts and The London Genome Centre
- British Heart Foundation Chairholders
- MRC [G0400874, G9521010] Funding Source: UKRI
- Medical Research Council [G0400874, G9521010, G9817803B] Funding Source: researchfish
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Hypertension is a complex disease that affects a large proportion of adult population. Although approximately half of the inter-individual variance in blood pressure (BP) level is heritable, identification of genes responsible for its regulation has remained challenging. Genome-wide association study (GWAS) is a novel approach to search for genetic variants contributing to complex diseases. We conducted GWAS for three BP traits [systolic and diastolic blood pressure (SBP and DBP); hypertension (HYP)] in the Kooperative Gesundheitsforschung in der Region Augsburg (KORA) S3 cohort (n = 1644) recruited from general population in Southern Germany. GWAS with 395 912 single nucleotide polymorphisms (SNPs) identified an association between BP traits and a common variant rs11646213 (T/A) upstream of the CDH13 gene at 16q23.3. The initial associations with HYP and DBP were confirmed in two other European population-based cohorts: KORA S4 (Germans) and HYPEST (Estonians). The associations between rs11646213 and three BP traits were replicated in combined analyses (dominant model: DBP, P = 5.55 x 10(-5), effect -1.40 mmHg; SBP, P = 0.007, effect -1.56 mmHg; HYP, P = 5.30 x 10(-8), OR = 0.67). Carriers of the minor allele A had a decreased risk of hypertension. A non-significant trend for association was also detected with severe family based hypertension in the BRIGHT sample (British). The novel susceptibility locus, CDH13, encodes for an adhesion glycoprotein T-cadherin, a regulator of vascular wall remodeling and angiogenesis. Its function is compatible with the BP biology and may improve the understanding of the pathogenesis of hypertension.
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