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      Haplotype-based case-control study of the association between the guanylate cyclase activator 2B (GUCA2B, Uroguanylin) gene and essential hypertension.

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          Abstract

          Uroguanylin (gene name: guanylate cyclase activator 2B, GUCA2B) is a peptide regulator of intestinal salt and water transport. It has been reported that the uroguanylin knockout mouse exhibits elevated blood pressure. Therefore, the GUCA2B gene is thought to be a susceptibility gene for essential hypertension (EH). Despite extensive studies, however, the relationship between the GUCA2B gene and EH has not yet been defined. The aim of this study was to assess the association between the human GUCA2B gene and EH. Using four single nucleotide polymorphisms (SNPs), we conducted a genetic association study in 281 EH patients and 279 age-matched normotensive (NT1) individuals. To derive more reliable data, we performed a duplicate case-control study in which we recruited another normotensive group (NT2). There was no significant difference in the overall distribution of alleles for any of the SNPs between the EH and NT1 groups, or between the EH and NT2 groups. Therefore, these four SNPs cannot be the genetic markers for EH. The occurrences of the C-A haplotype (rs883062-rs1047047) and the C-A-G haplotype (rs883062-rs1047047-rs2297566) were significantly higher in the EH group than in the NT1 group (p<0.0001) or the NT2 group (p<0.0001). These results suggest that the C-A haplotype and the C-A-G haplotype of the GUCA2B gene are the genetic markers for EH, and that GUCA2B or a neighboring gene might be a susceptibility gene for EH.

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          Author and article information

          Journal
          Hypertens. Res.
          Hypertension research : official journal of the Japanese Society of Hypertension
          Japanese Society of Hypertension
          0916-9636
          0916-9636
          Sep 2007
          : 30
          : 9
          Affiliations
          [1 ] Division of Molecular Diagnostics, Department of Advanced Medical Science, Nihon University School of Medicine, Tokyo, Japan.
          Article
          JST.JSTAGE/hypres/30.789
          10.1291/hypres.30.789
          18037771
          ee022e4c-69e4-4bc3-9f7a-0593be93e0c2
          History

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