Evidence from single nucleotide polymorphism analyses of ADVANCE study demonstrates EFNB3 as a hypertension risk gene

Johanne Tremblay; Yujia Wang; John Raelson; Francois Christophe Marois-Blanchet; Zenghui Wu; Hongyu Luo; Edward Bradley; John Chalmers; Mark Woodward; Stephen Harrap; Pavel Hamet; Jiangping Wu

doi:10.1038/srep44114

Evidence from single nucleotide polymorphism analyses of ADVANCE study demonstrates EFNB3 as a hypertension risk gene

Johanne Tremblay, Yujia Wang, John Raelson, Francois Christophe Marois-Blanchet, Zenghui Wu, Hongyu Luo, Edward Bradley, John Chalmers, Mark Woodward, Stephen Harrap, Pavel Hamet, Jiangping Wu

Bloomberg School of Public Health

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

EPH kinases and their ligands, ephrins (EFNs), have vital and diverse biological functions. We recently reported that Efnb3 gene deletion results in hypertension in female but not male mice. These data suggest that EFNB3 regulates blood pressure in a sex- and sex hormone-dependent way. In the present study, we conducted a human genetic study to assess the association of EFNB3 single nucleotide polymorphisms with human hypertension risks, using 3,448 patients with type 2 diabetes from the ADVANCE study (Action in Diabetes and Vascular Disease: Peterax and Diamicron MR Controlled Evaluation). We have observed significant association between 2 SNPs in the 3′ untranslated region or within the adjacent region just 3′ of the EFNB3 gene with hypertension, corroborating our findings from the mouse model. Thus, our investigation has shown that EFNB3 is a hypertension risk gene in certain individuals.

Original language	English (US)
Article number	44114
Journal	Scientific reports
Volume	7
DOIs	https://doi.org/10.1038/srep44114
State	Published - Mar 8 2017

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title = "Evidence from single nucleotide polymorphism analyses of ADVANCE study demonstrates EFNB3 as a hypertension risk gene",

abstract = "EPH kinases and their ligands, ephrins (EFNs), have vital and diverse biological functions. We recently reported that Efnb3 gene deletion results in hypertension in female but not male mice. These data suggest that EFNB3 regulates blood pressure in a sex- and sex hormone-dependent way. In the present study, we conducted a human genetic study to assess the association of EFNB3 single nucleotide polymorphisms with human hypertension risks, using 3,448 patients with type 2 diabetes from the ADVANCE study (Action in Diabetes and Vascular Disease: Peterax and Diamicron MR Controlled Evaluation). We have observed significant association between 2 SNPs in the 3′ untranslated region or within the adjacent region just 3′ of the EFNB3 gene with hypertension, corroborating our findings from the mouse model. Thus, our investigation has shown that EFNB3 is a hypertension risk gene in certain individuals.",

author = "Johanne Tremblay and Yujia Wang and John Raelson and Marois-Blanchet, {Francois Christophe} and Zenghui Wu and Hongyu Luo and Edward Bradley and John Chalmers and Mark Woodward and Stephen Harrap and Pavel Hamet and Jiangping Wu",

note = "Funding Information: The authors thank Jerry Pelletier (Biochemistry, McGill) for help in analyzing RNA motifs in the 3{\OE} UTR of EFNB3. This work was supported by grants from the Canadian Institutes of Health Research to J.W. (MOP57697, MOP69089 and MOP 123389), H.L. (MOP97829), JT and P.H (ISO106797). It was also financed by grants from the Natural Sciences and Engineering Research Council of Canada (203906-2012), Juvenile Diabetes Research Foundation (17-2013-440), Fonds de recherche du Quebec-Sante (Ag-06) and the J.-Louis Levesque Foundation to J.W. It is financed also by grants from OPTI-THERA to J.T. and P.H. Publisher Copyright: {\textcopyright} The Author(s) 2017.",

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doi = "10.1038/srep44114",

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T1 - Evidence from single nucleotide polymorphism analyses of ADVANCE study demonstrates EFNB3 as a hypertension risk gene

AU - Tremblay, Johanne

AU - Wang, Yujia

AU - Raelson, John

AU - Marois-Blanchet, Francois Christophe

AU - Wu, Zenghui

AU - Luo, Hongyu

AU - Bradley, Edward

AU - Chalmers, John

AU - Woodward, Mark

AU - Harrap, Stephen

AU - Hamet, Pavel

AU - Wu, Jiangping

N1 - Funding Information: The authors thank Jerry Pelletier (Biochemistry, McGill) for help in analyzing RNA motifs in the 3Œ UTR of EFNB3. This work was supported by grants from the Canadian Institutes of Health Research to J.W. (MOP57697, MOP69089 and MOP 123389), H.L. (MOP97829), JT and P.H (ISO106797). It was also financed by grants from the Natural Sciences and Engineering Research Council of Canada (203906-2012), Juvenile Diabetes Research Foundation (17-2013-440), Fonds de recherche du Quebec-Sante (Ag-06) and the J.-Louis Levesque Foundation to J.W. It is financed also by grants from OPTI-THERA to J.T. and P.H. Publisher Copyright: © The Author(s) 2017.

PY - 2017/3/8

Y1 - 2017/3/8

N2 - EPH kinases and their ligands, ephrins (EFNs), have vital and diverse biological functions. We recently reported that Efnb3 gene deletion results in hypertension in female but not male mice. These data suggest that EFNB3 regulates blood pressure in a sex- and sex hormone-dependent way. In the present study, we conducted a human genetic study to assess the association of EFNB3 single nucleotide polymorphisms with human hypertension risks, using 3,448 patients with type 2 diabetes from the ADVANCE study (Action in Diabetes and Vascular Disease: Peterax and Diamicron MR Controlled Evaluation). We have observed significant association between 2 SNPs in the 3′ untranslated region or within the adjacent region just 3′ of the EFNB3 gene with hypertension, corroborating our findings from the mouse model. Thus, our investigation has shown that EFNB3 is a hypertension risk gene in certain individuals.

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Evidence from single nucleotide polymorphism analyses of ADVANCE study demonstrates EFNB3 as a hypertension risk gene

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