The NHLBI Family Blood Pressure Program is made up of four cooperating networks whose overall objective is to localize and characterize genes contributing to variation in blood pressure levels and hypertension status. The four networks were originally separately funded and competitive, but two critical realizations have led to full cooperation and collaboration. First, the oligogenic nature of blood pressure control dictates that large samples are necessary to achieve adequate statistical power for genomic linkage and association analyses. Second, linkage intervals are broad and contain large numbers of genes, so that success in identifying genes and mutations requires the effort of multiple laboratories freely sharing information. This coordination extends far beyond phenotyping and genotyping and is best exemplified by the Program's creation of a pooled data set and agreements about coordinated publications. During the initial funding period, the Program surpassed its original recruitment goals, carried out multiple genome-wide linkage and association analyses and created an interim pooled data set consisting of phenotype and genotype data from more than 10,000 individuals. In this renewal application, the Program proposes five specific aims to be carried out by all four networks.
These aims can be grouped according to two complementary themes: First, these applicants will create and analyze a database of blood pressure- related phenotype and genotype data from all FBPP participants (Aim 1). Within linked regions, they will identify allelic variation within positional candidate genes and evaluate the relationship of these polymorphisms with blood pressure levels and hypertension status (Aims 2 and 3). Second, they will use quantitative measures of target organ damage to identify genes that influence susceptibility to develop hypertensive heart and kidney diseases (Aims 4 and 5). In addition to the Program specific aims, each network proposes specific aims to be carried out by that network alone, based on unique aspects of their population and interests and expertise of the investigators. The Family Blood Pressure Program represents the most determined multidisciplinary approach to the genetics of hypertension ever assembled. The resulting synthesis of ideas and amassed data permits rigorous hypothesis testing not otherwise possible and will hasten understanding of the previously elusive genetic variation responsible for disease risk.
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| Weissgerber, Tracey L; Turner, Stephen T; Mosley Jr, Thomas H et al. (2016) Hypertension in Pregnancy and Future Cardiovascular Event Risk in Siblings. J Am Soc Nephrol 27:894-902 |
| Scantlebury, Dawn C; Kane, Garvan C; Wiste, Heather J et al. (2015) Left ventricular hypertrophy after hypertensive pregnancy disorders. Heart 101:1584-90 |
| Weissgerber, Tracey L; Milic, Natasa M; Turner, Stephen T et al. (2015) Uric Acid: A Missing Link Between Hypertensive Pregnancy Disorders and Future Cardiovascular Disease? Mayo Clin Proc 90:1207-16 |
| Simino, Jeannette; Kume, Rezart; Kraja, Aldi T et al. (2014) Linkage analysis incorporating gene-age interactions identifies seven novel lipid loci: the Family Blood Pressure Program. Atherosclerosis 235:84-93 |
| Brown, Catherine M; Turner, Stephen T; Bailey, Kent R et al. (2013) Hypertension in pregnancy is associated with elevated C-reactive protein levels later in life. J Hypertens 31:2213-9; discussion 2219 |
| Weissgerber, Tracey L; Turner, Stephen T; Bailey, Kent R et al. (2013) Hypertension in pregnancy is a risk factor for peripheral arterial disease decades after pregnancy. Atherosclerosis 229:212-6 |
| White, Wendy M; Turner, Stephen T; Bailey, Kent R et al. (2013) Hypertension in pregnancy is associated with elevated homocysteine levels later in life. Am J Obstet Gynecol 209:454.e1-7 |
| Monda, Keri L; Chen, Gary K; Taylor, Kira C et al. (2013) A meta-analysis identifies new loci associated with body mass index in individuals of African ancestry. Nat Genet 45:690-6 |
| Kattah, Andrea G; Asad, Reem; Scantlebury, Dawn C et al. (2013) Hypertension in pregnancy is a risk factor for microalbuminuria later in life. J Clin Hypertens (Greenwich) 15:617-23 |
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