Arterial Properties in Relation to Genetic Variations in the Adducin Subunits in a White Population
Background Adducin is a membrane skeleton protein, which consists of either α- and β- or α- and γ-subunits. We investigated whether arterial characteristics might be related to the genes encoding ADD1 (Gly460Trp-rs4961), ADD2 (C1797T-rs4984), and ADD3 (IVS11+386A>G-rs3731566). Methods We randomly...
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creator | Seidlerová, Jitka Staessen, Jan A. Bochud, Murielle Nawrot, Tim Casamassima, Nunzia Citterio, Lorena Kuznetsova, Tatiana Jin, Yu Manunta, Paulo Richart, Tom Struijker-Boudier, Harry A. Fagard, Robert Filipovský, Jan Bianchi, Giuseppe |
description | Background Adducin is a membrane skeleton protein, which consists of either α- and β- or α- and γ-subunits. We investigated whether arterial characteristics might be related to the genes encoding ADD1 (Gly460Trp-rs4961), ADD2 (C1797T-rs4984), and ADD3 (IVS11+386A>G-rs3731566). Methods We randomly recruited 1,126 Flemish subjects (mean age, 43.8 years; 50.3% women). Using a wall-tracking ultrasound system, we measured the properties of the carotid, femoral, and brachial arteries. We studied multivariate-adjusted phenotype–genotype associations, using a population- and family-based approach. Results In single-gene analyses, brachial diameter was 0.15 mm (P = 0.0022) larger, and brachial distensibility and cross-sectional compliance were 1.55 × 10–3/kPa (P = 0.013) and 0.017 mm2/kPa (P = 0.0029) lower in ADD3 AA than ADD3 GG homozygotes with an additive effect of the G allele. In multiple-gene analyses, the association of brachial diameter and distensibility with the ADD3 G allele occurred only in ADD1 GlyGly homozygotes. Otherwise, the associations between the arterial phenotypes in the three vascular beds and the ADD1 or ADD2 polymorphisms were not significant. In family-based analyses, the multivariate-adjusted heritability was 0.52, 0.38, and 0.30 for brachial diameter, distensibility, and cross-sectional compliance, respectively (P < 0.001). There was no evidence for population stratification (0.07 ≤ P ≤ 0.96). Transmission of the mutated ADD3 G allele was associated with smaller brachial diameter in 342 informative offspring (–0.12 ± 0.04 mm; P = 0.0085) and in 209 offspring, who were ADD1 GlyGly homozygotes (–0.14 ± 0.06 mm; P = 0.018). Conclusions In ADD1 GlyGly homozygotes, the properties of the brachial artery are related to the ADD3 (A386G) polymorphism, but the underlying mechanism needs further clarification. American Journal of Hypertension (2009). doi: 10.1038/ajh.2008.261 |
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We investigated whether arterial characteristics might be related to the genes encoding ADD1 (Gly460Trp-rs4961), ADD2 (C1797T-rs4984), and ADD3 (IVS11+386A>G-rs3731566). Methods We randomly recruited 1,126 Flemish subjects (mean age, 43.8 years; 50.3% women). Using a wall-tracking ultrasound system, we measured the properties of the carotid, femoral, and brachial arteries. We studied multivariate-adjusted phenotype–genotype associations, using a population- and family-based approach. Results In single-gene analyses, brachial diameter was 0.15 mm (P = 0.0022) larger, and brachial distensibility and cross-sectional compliance were 1.55 × 10–3/kPa (P = 0.013) and 0.017 mm2/kPa (P = 0.0029) lower in ADD3 AA than ADD3 GG homozygotes with an additive effect of the G allele. In multiple-gene analyses, the association of brachial diameter and distensibility with the ADD3 G allele occurred only in ADD1 GlyGly homozygotes. Otherwise, the associations between the arterial phenotypes in the three vascular beds and the ADD1 or ADD2 polymorphisms were not significant. In family-based analyses, the multivariate-adjusted heritability was 0.52, 0.38, and 0.30 for brachial diameter, distensibility, and cross-sectional compliance, respectively (P < 0.001). There was no evidence for population stratification (0.07 ≤ P ≤ 0.96). Transmission of the mutated ADD3 G allele was associated with smaller brachial diameter in 342 informative offspring (–0.12 ± 0.04 mm; P = 0.0085) and in 209 offspring, who were ADD1 GlyGly homozygotes (–0.14 ± 0.06 mm; P = 0.018). Conclusions In ADD1 GlyGly homozygotes, the properties of the brachial artery are related to the ADD3 (A386G) polymorphism, but the underlying mechanism needs further clarification. American Journal of Hypertension (2009). doi: 10.1038/ajh.2008.261</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1941-7225</identifier><identifier>EISSN: 1879-1905</identifier><identifier>DOI: 10.1038/ajh.2008.261</identifier><identifier>PMID: 18787518</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Basingstoke: Oxford University Press</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Arterial hypertension. Arterial hypotension ; Belgium - epidemiology ; Biological and medical sciences ; Blood and lymphatic vessels ; Brachial Artery - diagnostic imaging ; Brachial Artery - physiopathology ; Calmodulin-Binding Proteins - genetics ; Cardiology. Vascular system ; Carotid Arteries - diagnostic imaging ; Carotid Arteries - physiopathology ; Child ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Cytoskeletal Proteins ; DNA - genetics ; European Continental Ancestry Group ; Female ; Femoral Artery - diagnostic imaging ; Femoral Artery - physiopathology ; Genetic Variation ; Humans ; Hypertension - ethnology ; Hypertension - genetics ; Hypertension - physiopathology ; Male ; Medical sciences ; Middle Aged ; Polymerase Chain Reaction ; Retrospective Studies ; Ultrasonography ; Vascular Resistance - genetics ; Young Adult</subject><ispartof>American journal of hypertension, 2009-01, Vol.22 (1), p.21-26</ispartof><rights>American Journal of Hypertension, Ltd. © 2009 by the American Journal of Hypertension, Ltd. 2009</rights><rights>2009 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-95df3330f835057b322b54fea3ae3982cf6a513ef06d57698e431e5704a7022e3</citedby><cites>FETCH-LOGICAL-c455t-95df3330f835057b322b54fea3ae3982cf6a513ef06d57698e431e5704a7022e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4009,27902,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21152071$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18787518$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seidlerová, Jitka</creatorcontrib><creatorcontrib>Staessen, Jan A.</creatorcontrib><creatorcontrib>Bochud, Murielle</creatorcontrib><creatorcontrib>Nawrot, Tim</creatorcontrib><creatorcontrib>Casamassima, Nunzia</creatorcontrib><creatorcontrib>Citterio, Lorena</creatorcontrib><creatorcontrib>Kuznetsova, Tatiana</creatorcontrib><creatorcontrib>Jin, Yu</creatorcontrib><creatorcontrib>Manunta, Paulo</creatorcontrib><creatorcontrib>Richart, Tom</creatorcontrib><creatorcontrib>Struijker-Boudier, Harry A.</creatorcontrib><creatorcontrib>Fagard, Robert</creatorcontrib><creatorcontrib>Filipovský, Jan</creatorcontrib><creatorcontrib>Bianchi, Giuseppe</creatorcontrib><title>Arterial Properties in Relation to Genetic Variations in the Adducin Subunits in a White Population</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Background Adducin is a membrane skeleton protein, which consists of either α- and β- or α- and γ-subunits. We investigated whether arterial characteristics might be related to the genes encoding ADD1 (Gly460Trp-rs4961), ADD2 (C1797T-rs4984), and ADD3 (IVS11+386A>G-rs3731566). Methods We randomly recruited 1,126 Flemish subjects (mean age, 43.8 years; 50.3% women). Using a wall-tracking ultrasound system, we measured the properties of the carotid, femoral, and brachial arteries. We studied multivariate-adjusted phenotype–genotype associations, using a population- and family-based approach. Results In single-gene analyses, brachial diameter was 0.15 mm (P = 0.0022) larger, and brachial distensibility and cross-sectional compliance were 1.55 × 10–3/kPa (P = 0.013) and 0.017 mm2/kPa (P = 0.0029) lower in ADD3 AA than ADD3 GG homozygotes with an additive effect of the G allele. In multiple-gene analyses, the association of brachial diameter and distensibility with the ADD3 G allele occurred only in ADD1 GlyGly homozygotes. Otherwise, the associations between the arterial phenotypes in the three vascular beds and the ADD1 or ADD2 polymorphisms were not significant. In family-based analyses, the multivariate-adjusted heritability was 0.52, 0.38, and 0.30 for brachial diameter, distensibility, and cross-sectional compliance, respectively (P < 0.001). There was no evidence for population stratification (0.07 ≤ P ≤ 0.96). Transmission of the mutated ADD3 G allele was associated with smaller brachial diameter in 342 informative offspring (–0.12 ± 0.04 mm; P = 0.0085) and in 209 offspring, who were ADD1 GlyGly homozygotes (–0.14 ± 0.06 mm; P = 0.018). Conclusions In ADD1 GlyGly homozygotes, the properties of the brachial artery are related to the ADD3 (A386G) polymorphism, but the underlying mechanism needs further clarification. American Journal of Hypertension (2009). doi: 10.1038/ajh.2008.261</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Belgium - epidemiology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Brachial Artery - diagnostic imaging</subject><subject>Brachial Artery - physiopathology</subject><subject>Calmodulin-Binding Proteins - genetics</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Arteries - diagnostic imaging</subject><subject>Carotid Arteries - physiopathology</subject><subject>Child</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Cytoskeletal Proteins</subject><subject>DNA - genetics</subject><subject>European Continental Ancestry Group</subject><subject>Female</subject><subject>Femoral Artery - diagnostic imaging</subject><subject>Femoral Artery - physiopathology</subject><subject>Genetic Variation</subject><subject>Humans</subject><subject>Hypertension - ethnology</subject><subject>Hypertension - genetics</subject><subject>Hypertension - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymerase Chain Reaction</subject><subject>Retrospective Studies</subject><subject>Ultrasonography</subject><subject>Vascular Resistance - genetics</subject><subject>Young Adult</subject><issn>0895-7061</issn><issn>1941-7225</issn><issn>1879-1905</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqF0Ntr1EAUBvBBLHZbffNZAtL60qxzyVzyuBRtlYKlRi2-DLPJCTtrNhPnAvrfO9ssFXzx6QyHH98cPoReErwkmKm3ZrtZUozVkgryBC1IXZFSUsqfogVWNS8lFuQYnYSwxRhXQpBn6JgoqSQnaoHalY_grRmKW-8m8NFCKOxY3MFgonVjEV1xBSNE2xZfTYb75YOIGyhWXZfa_P6c1mm08WFvim8bG6G4dVOaM56jo94MAV4c5in68v5dc3ld3ny6-nC5uinbivNY1rzrGWO4V4xjLteM0jWvejDMAKsVbXthOGHQY9FxKWoFFSPAJa6MxJQCO0Xnc-7k3c8EIeqdDS0MgxnBpaCFkJXEjGT4-h-4dcmP-TZNMK0UY0qorC5m1XoXgodeT97ujP-dkd5Xr3P1el-9ztVn_uoQmtY76P7iQ9cZnB2ACa0Zem_G1oZHRwnhFMt90JvZuTT978tyljZE-PVojf-hhWSS6-v77_ru_qNoGtnohv0BbhmmVQ</recordid><startdate>200901</startdate><enddate>200901</enddate><creator>Seidlerová, Jitka</creator><creator>Staessen, Jan A.</creator><creator>Bochud, Murielle</creator><creator>Nawrot, Tim</creator><creator>Casamassima, Nunzia</creator><creator>Citterio, Lorena</creator><creator>Kuznetsova, Tatiana</creator><creator>Jin, Yu</creator><creator>Manunta, Paulo</creator><creator>Richart, Tom</creator><creator>Struijker-Boudier, Harry A.</creator><creator>Fagard, Robert</creator><creator>Filipovský, Jan</creator><creator>Bianchi, Giuseppe</creator><general>Oxford University Press</general><general>Nature Publishing Group</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>200901</creationdate><title>Arterial Properties in Relation to Genetic Variations in the Adducin Subunits in a White Population</title><author>Seidlerová, Jitka ; Staessen, Jan A. ; Bochud, Murielle ; Nawrot, Tim ; Casamassima, Nunzia ; Citterio, Lorena ; Kuznetsova, Tatiana ; Jin, Yu ; Manunta, Paulo ; Richart, Tom ; Struijker-Boudier, Harry A. ; Fagard, Robert ; Filipovský, Jan ; Bianchi, Giuseppe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-95df3330f835057b322b54fea3ae3982cf6a513ef06d57698e431e5704a7022e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Belgium - epidemiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Brachial Artery - diagnostic imaging</topic><topic>Brachial Artery - physiopathology</topic><topic>Calmodulin-Binding Proteins - genetics</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Arteries - diagnostic imaging</topic><topic>Carotid Arteries - physiopathology</topic><topic>Child</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Cytoskeletal Proteins</topic><topic>DNA - genetics</topic><topic>European Continental Ancestry Group</topic><topic>Female</topic><topic>Femoral Artery - diagnostic imaging</topic><topic>Femoral Artery - physiopathology</topic><topic>Genetic Variation</topic><topic>Humans</topic><topic>Hypertension - ethnology</topic><topic>Hypertension - genetics</topic><topic>Hypertension - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymerase Chain Reaction</topic><topic>Retrospective Studies</topic><topic>Ultrasonography</topic><topic>Vascular Resistance - genetics</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seidlerová, Jitka</creatorcontrib><creatorcontrib>Staessen, Jan A.</creatorcontrib><creatorcontrib>Bochud, Murielle</creatorcontrib><creatorcontrib>Nawrot, Tim</creatorcontrib><creatorcontrib>Casamassima, Nunzia</creatorcontrib><creatorcontrib>Citterio, Lorena</creatorcontrib><creatorcontrib>Kuznetsova, Tatiana</creatorcontrib><creatorcontrib>Jin, Yu</creatorcontrib><creatorcontrib>Manunta, Paulo</creatorcontrib><creatorcontrib>Richart, Tom</creatorcontrib><creatorcontrib>Struijker-Boudier, Harry A.</creatorcontrib><creatorcontrib>Fagard, Robert</creatorcontrib><creatorcontrib>Filipovský, Jan</creatorcontrib><creatorcontrib>Bianchi, Giuseppe</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seidlerová, Jitka</au><au>Staessen, Jan A.</au><au>Bochud, Murielle</au><au>Nawrot, Tim</au><au>Casamassima, Nunzia</au><au>Citterio, Lorena</au><au>Kuznetsova, Tatiana</au><au>Jin, Yu</au><au>Manunta, Paulo</au><au>Richart, Tom</au><au>Struijker-Boudier, Harry A.</au><au>Fagard, Robert</au><au>Filipovský, Jan</au><au>Bianchi, Giuseppe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arterial Properties in Relation to Genetic Variations in the Adducin Subunits in a White Population</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2009-01</date><risdate>2009</risdate><volume>22</volume><issue>1</issue><spage>21</spage><epage>26</epage><pages>21-26</pages><issn>0895-7061</issn><eissn>1941-7225</eissn><eissn>1879-1905</eissn><coden>AJHYE6</coden><abstract>Background Adducin is a membrane skeleton protein, which consists of either α- and β- or α- and γ-subunits. We investigated whether arterial characteristics might be related to the genes encoding ADD1 (Gly460Trp-rs4961), ADD2 (C1797T-rs4984), and ADD3 (IVS11+386A>G-rs3731566). Methods We randomly recruited 1,126 Flemish subjects (mean age, 43.8 years; 50.3% women). Using a wall-tracking ultrasound system, we measured the properties of the carotid, femoral, and brachial arteries. We studied multivariate-adjusted phenotype–genotype associations, using a population- and family-based approach. Results In single-gene analyses, brachial diameter was 0.15 mm (P = 0.0022) larger, and brachial distensibility and cross-sectional compliance were 1.55 × 10–3/kPa (P = 0.013) and 0.017 mm2/kPa (P = 0.0029) lower in ADD3 AA than ADD3 GG homozygotes with an additive effect of the G allele. In multiple-gene analyses, the association of brachial diameter and distensibility with the ADD3 G allele occurred only in ADD1 GlyGly homozygotes. Otherwise, the associations between the arterial phenotypes in the three vascular beds and the ADD1 or ADD2 polymorphisms were not significant. In family-based analyses, the multivariate-adjusted heritability was 0.52, 0.38, and 0.30 for brachial diameter, distensibility, and cross-sectional compliance, respectively (P < 0.001). There was no evidence for population stratification (0.07 ≤ P ≤ 0.96). Transmission of the mutated ADD3 G allele was associated with smaller brachial diameter in 342 informative offspring (–0.12 ± 0.04 mm; P = 0.0085) and in 209 offspring, who were ADD1 GlyGly homozygotes (–0.14 ± 0.06 mm; P = 0.018). Conclusions In ADD1 GlyGly homozygotes, the properties of the brachial artery are related to the ADD3 (A386G) polymorphism, but the underlying mechanism needs further clarification. American Journal of Hypertension (2009). doi: 10.1038/ajh.2008.261</abstract><cop>Basingstoke</cop><pub>Oxford University Press</pub><pmid>18787518</pmid><doi>10.1038/ajh.2008.261</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Aged, 80 and over Arterial hypertension. Arterial hypotension Belgium - epidemiology Biological and medical sciences Blood and lymphatic vessels Brachial Artery - diagnostic imaging Brachial Artery - physiopathology Calmodulin-Binding Proteins - genetics Cardiology. Vascular system Carotid Arteries - diagnostic imaging Carotid Arteries - physiopathology Child Clinical manifestations. Epidemiology. Investigative techniques. Etiology Cytoskeletal Proteins DNA - genetics European Continental Ancestry Group Female Femoral Artery - diagnostic imaging Femoral Artery - physiopathology Genetic Variation Humans Hypertension - ethnology Hypertension - genetics Hypertension - physiopathology Male Medical sciences Middle Aged Polymerase Chain Reaction Retrospective Studies Ultrasonography Vascular Resistance - genetics Young Adult |
title | Arterial Properties in Relation to Genetic Variations in the Adducin Subunits in a White Population |
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