4.3 Article

Prostasin: A possible candidate gene for human hypertension

期刊

AMERICAN JOURNAL OF HYPERTENSION
卷 21, 期 9, 页码 1028-1033

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OXFORD UNIV PRESS
DOI: 10.1038/ajh.2008.224

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  1. National Heart, Lung, and Blood Institute [HL77230, HL076723, HL85817, HL69999]
  2. American Heart Association [0430078N, 0435146N]
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL069999, R21HL076723, R21HL085817, R01HL077230] Funding Source: NIH RePORTER

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BACKGROUND Prostasin, a serine protease, is suggested to be a novel mechanism regulating the epithelial sodium channel (ENaC) expressed in the distal nephron. This study aimed to evaluate whether the human prostasin gene is a novel candidate gene underlying blood pressure (BP) elevation. METHODS In a sample of healthy African-American (AA) and European-American (EA) twin subjects aged 17.6 +/- 3.3 years (n = 920,45% AAs), race-specific tagging single-nucleotide polymorphisms (tSNPs) were identified to tag all the available SNPs +/- 2 kb up- and downstream of the prostasin gene from HapMap at r(2) of 0.8-1.0. Selection yielded four tSNPs in AAs and one in EAs, with one tSNP (rs12597511:C to T) present in both AAs and EAs. RESULTS For 12597511, CT and TT genotypes exhibited higher systolic BP (SBP) than CC genotype (115.9 +/- 1.1 mm Hg vs. 113.7 +/- 0.6 mm Hg, P = 0.025 (AAs); and 110.7 +/- 0.5 mm Hg vs. 109.6 +/- 0.6 mm Hg, P = 0.115 (EAs)). CT and TT genotypes compared with CC genotype showed a significant increase in diastolic BP (DBP) in both racial groups (62.5 +/- 0.7 mm Hg vs. 60.4 +/- 0.4 mm Hg, P = 0.003 (AAs); and 58.2 +/- 0.3 mm Hg vs. 56.7 +/- 0.4 mm Hg, P = 0.007 (EAs)). Furthermore, there was an increase in radial pulse wave velocity (PWV) in subjects with CT and TT genotype as compared with those with CC genotype (6.5 +/- 0.1 vs. 6.1 +/- 0.1 m/s, P < 0.0001) (EAs); and 6.7 +/- 0.1 vs. 6.6 +/- 0.1 m/s P = 0.354 (AAs)). Analyses combining AAs and EAs consistently demonstrated a statistical significance of rs12597511 on all the phenotypes including SBP/DBP and PWV. CONCLUSION Genetic variation of the prostasin gene may be implicated in the development of hypertension in youths.

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