Genome-wide linkage analysis of systolic and diastolic blood pressure : The Québec Family Study
Blood pressure (BP), an important risk factor for coronary heart disease, is a complex trait with multiple genetic etiologies. While some loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals that can be detected with a genome scan approach. A genome-wide...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2000-10, Vol.102 (16), p.1956-1963 |
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| container_issue | 16 |
| container_start_page | 1956 |
| container_title | Circulation (New York, N.Y.) |
| container_volume | 102 |
| creator | RICE, Treva RANKINEN, Tuomo PROVINCE, Michael A CHAGNON, Yvon C PERUSSE, Louis BORECKI, Ingrid B BOUCHARD, Claude RAO, D. C |
| description | Blood pressure (BP), an important risk factor for coronary heart disease, is a complex trait with multiple genetic etiologies. While some loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals that can be detected with a genome scan approach.
A genome-wide scan was performed in 125 random and 81 obese families participating in the Québec Family Study. A multipoint variance-components linkage analysis of 420 markers (353 microsatellites and 67 restriction fragment length polymorphisms) revealed several signals (P: |
| doi_str_mv | 10.1161/01.CIR.102.16.1956 |
| format | Article |
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A genome-wide scan was performed in 125 random and 81 obese families participating in the Québec Family Study. A multipoint variance-components linkage analysis of 420 markers (353 microsatellites and 67 restriction fragment length polymorphisms) revealed several signals (P:<0.0023) for systolic BP on 1p (D1S551, ATP1A1), 2p (D2S1790, D2S2972), 5p (D5S1986), 7q (D7S530), 8q (CRH), and 19p (D19S247). Suggestive evidence (0.0023<P:<0.01) was found on 3q, 10p, 12p, 14q, and 22q. The results were encouraging for HSD3B1 (P:<0.03), AGT (P:<0.03), ACE (P:<0.02), and adipsin (P:<0.005) but null with regard to other candidates (eg, renin, and glucocorticoid and adrenergic receptors).
Multiple linkage regions support the notion that risk for hypertension is due to multiple (ie, oligogenic) susceptibility loci. Comparisons across the complete, random, and obese samples suggest that some regions are specific to BP and others may involve obesity (eg, pleiotropy, epistasis, or gene-environment interaction). Some of these areas harbor known candidates. Others involve novel regions, some of which replicate previous reports and provide a focus for future studies to identify novel genes that influence interindividual variation in BP.]]></description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.102.16.1956</identifier><identifier>PMID: 11034945</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Age Distribution ; Aged ; Biological and medical sciences ; Blood Pressure - genetics ; Body Mass Index ; Cardiology. Vascular system ; Chromosome Mapping ; Coronary heart disease ; Diastole - genetics ; Female ; Genetic Linkage ; Genetic Variation ; Genome, Human ; Heart ; Humans ; Hypertension - epidemiology ; Hypertension - genetics ; Lod Score ; Male ; Medical sciences ; Microsatellite Repeats ; Middle Aged ; Obesity - epidemiology ; Obesity - genetics ; Physical Chromosome Mapping ; Polymorphism, Restriction Fragment Length ; Quantitative Trait, Heritable ; Quebec - epidemiology ; Regression Analysis ; Sex Distribution ; Systole - genetics</subject><ispartof>Circulation (New York, N.Y.), 2000-10, Vol.102 (16), p.1956-1963</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 17, 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1530328$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11034945$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RICE, Treva</creatorcontrib><creatorcontrib>RANKINEN, Tuomo</creatorcontrib><creatorcontrib>PROVINCE, Michael A</creatorcontrib><creatorcontrib>CHAGNON, Yvon C</creatorcontrib><creatorcontrib>PERUSSE, Louis</creatorcontrib><creatorcontrib>BORECKI, Ingrid B</creatorcontrib><creatorcontrib>BOUCHARD, Claude</creatorcontrib><creatorcontrib>RAO, D. C</creatorcontrib><title>Genome-wide linkage analysis of systolic and diastolic blood pressure : The Québec Family Study</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description><![CDATA[Blood pressure (BP), an important risk factor for coronary heart disease, is a complex trait with multiple genetic etiologies. While some loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals that can be detected with a genome scan approach.
A genome-wide scan was performed in 125 random and 81 obese families participating in the Québec Family Study. A multipoint variance-components linkage analysis of 420 markers (353 microsatellites and 67 restriction fragment length polymorphisms) revealed several signals (P:<0.0023) for systolic BP on 1p (D1S551, ATP1A1), 2p (D2S1790, D2S2972), 5p (D5S1986), 7q (D7S530), 8q (CRH), and 19p (D19S247). Suggestive evidence (0.0023<P:<0.01) was found on 3q, 10p, 12p, 14q, and 22q. The results were encouraging for HSD3B1 (P:<0.03), AGT (P:<0.03), ACE (P:<0.02), and adipsin (P:<0.005) but null with regard to other candidates (eg, renin, and glucocorticoid and adrenergic receptors).
Multiple linkage regions support the notion that risk for hypertension is due to multiple (ie, oligogenic) susceptibility loci. Comparisons across the complete, random, and obese samples suggest that some regions are specific to BP and others may involve obesity (eg, pleiotropy, epistasis, or gene-environment interaction). Some of these areas harbor known candidates. Others involve novel regions, some of which replicate previous reports and provide a focus for future studies to identify novel genes that influence interindividual variation in BP.]]></description><subject>Age Distribution</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - genetics</subject><subject>Body Mass Index</subject><subject>Cardiology. Vascular system</subject><subject>Chromosome Mapping</subject><subject>Coronary heart disease</subject><subject>Diastole - genetics</subject><subject>Female</subject><subject>Genetic Linkage</subject><subject>Genetic Variation</subject><subject>Genome, Human</subject><subject>Heart</subject><subject>Humans</subject><subject>Hypertension - epidemiology</subject><subject>Hypertension - genetics</subject><subject>Lod Score</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsatellite Repeats</subject><subject>Middle Aged</subject><subject>Obesity - epidemiology</subject><subject>Obesity - genetics</subject><subject>Physical Chromosome Mapping</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Quantitative Trait, Heritable</subject><subject>Quebec - epidemiology</subject><subject>Regression Analysis</subject><subject>Sex Distribution</subject><subject>Systole - genetics</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0E1KxEAQBeBGFB1HL-BCGhF3if2bTruTQUdBEHVcx0pS0dZOMqYnSI7kObyYAUcEV8UrPh5UEXLAWcx5wk8Zj2fX9zFnIuZJzK1ONsiEa6EipaXdJBPGmI2MFGKH7IbwOsZEGr1NdjhnUlmlJ-Rpjk1bY_ThSqTeNW_wjBQa8ENwgbYVDUNYtd4V47KkpYN1yn3blnTZYQh9h_SMLl6Q3vVfnzkW9BJq5wf6sOrLYY9sVeAD7q_nlDxeXixmV9HN7fx6dn4TvUiWrCKtTKqYrVIoFeQVgEIGCTBZKWNRoS5YlVs0IFIjeJ7rEnMNgidoWaoA5JSc_PQuu_a9x7DKahcK9B4abPuQGSGlMakZ4dE_-Nr23XhxyAQXRlvO7IgO16jPayyzZedq6Ibs93EjOF4DCAX4qoOmcOHPacmkSOU3Dyp9fA</recordid><startdate>20001017</startdate><enddate>20001017</enddate><creator>RICE, Treva</creator><creator>RANKINEN, Tuomo</creator><creator>PROVINCE, Michael A</creator><creator>CHAGNON, Yvon C</creator><creator>PERUSSE, Louis</creator><creator>BORECKI, Ingrid B</creator><creator>BOUCHARD, Claude</creator><creator>RAO, D. C</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20001017</creationdate><title>Genome-wide linkage analysis of systolic and diastolic blood pressure : The Québec Family Study</title><author>RICE, Treva ; RANKINEN, Tuomo ; PROVINCE, Michael A ; CHAGNON, Yvon C ; PERUSSE, Louis ; BORECKI, Ingrid B ; BOUCHARD, Claude ; RAO, D. C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h306t-5478409f8ad4abfaa4e0a6a03f479e4e5c0fb9e7a28721bb5deb5a216e9084aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Age Distribution</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - genetics</topic><topic>Body Mass Index</topic><topic>Cardiology. Vascular system</topic><topic>Chromosome Mapping</topic><topic>Coronary heart disease</topic><topic>Diastole - genetics</topic><topic>Female</topic><topic>Genetic Linkage</topic><topic>Genetic Variation</topic><topic>Genome, Human</topic><topic>Heart</topic><topic>Humans</topic><topic>Hypertension - epidemiology</topic><topic>Hypertension - genetics</topic><topic>Lod Score</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsatellite Repeats</topic><topic>Middle Aged</topic><topic>Obesity - epidemiology</topic><topic>Obesity - genetics</topic><topic>Physical Chromosome Mapping</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Quantitative Trait, Heritable</topic><topic>Quebec - epidemiology</topic><topic>Regression Analysis</topic><topic>Sex Distribution</topic><topic>Systole - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RICE, Treva</creatorcontrib><creatorcontrib>RANKINEN, Tuomo</creatorcontrib><creatorcontrib>PROVINCE, Michael A</creatorcontrib><creatorcontrib>CHAGNON, Yvon C</creatorcontrib><creatorcontrib>PERUSSE, Louis</creatorcontrib><creatorcontrib>BORECKI, Ingrid B</creatorcontrib><creatorcontrib>BOUCHARD, Claude</creatorcontrib><creatorcontrib>RAO, D. C</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>RICE, Treva</au><au>RANKINEN, Tuomo</au><au>PROVINCE, Michael A</au><au>CHAGNON, Yvon C</au><au>PERUSSE, Louis</au><au>BORECKI, Ingrid B</au><au>BOUCHARD, Claude</au><au>RAO, D. C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide linkage analysis of systolic and diastolic blood pressure : The Québec Family Study</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2000-10-17</date><risdate>2000</risdate><volume>102</volume><issue>16</issue><spage>1956</spage><epage>1963</epage><pages>1956-1963</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract><![CDATA[Blood pressure (BP), an important risk factor for coronary heart disease, is a complex trait with multiple genetic etiologies. While some loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals that can be detected with a genome scan approach.
A genome-wide scan was performed in 125 random and 81 obese families participating in the Québec Family Study. A multipoint variance-components linkage analysis of 420 markers (353 microsatellites and 67 restriction fragment length polymorphisms) revealed several signals (P:<0.0023) for systolic BP on 1p (D1S551, ATP1A1), 2p (D2S1790, D2S2972), 5p (D5S1986), 7q (D7S530), 8q (CRH), and 19p (D19S247). Suggestive evidence (0.0023<P:<0.01) was found on 3q, 10p, 12p, 14q, and 22q. The results were encouraging for HSD3B1 (P:<0.03), AGT (P:<0.03), ACE (P:<0.02), and adipsin (P:<0.005) but null with regard to other candidates (eg, renin, and glucocorticoid and adrenergic receptors).
Multiple linkage regions support the notion that risk for hypertension is due to multiple (ie, oligogenic) susceptibility loci. Comparisons across the complete, random, and obese samples suggest that some regions are specific to BP and others may involve obesity (eg, pleiotropy, epistasis, or gene-environment interaction). Some of these areas harbor known candidates. Others involve novel regions, some of which replicate previous reports and provide a focus for future studies to identify novel genes that influence interindividual variation in BP.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11034945</pmid><doi>10.1161/01.CIR.102.16.1956</doi><tpages>8</tpages></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2000-10, Vol.102 (16), p.1956-1963 |
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| source | MEDLINE; EZB Electronic Journals Library; American Heart Association; Journals@Ovid Complete |
| subjects | Age Distribution Aged Biological and medical sciences Blood Pressure - genetics Body Mass Index Cardiology. Vascular system Chromosome Mapping Coronary heart disease Diastole - genetics Female Genetic Linkage Genetic Variation Genome, Human Heart Humans Hypertension - epidemiology Hypertension - genetics Lod Score Male Medical sciences Microsatellite Repeats Middle Aged Obesity - epidemiology Obesity - genetics Physical Chromosome Mapping Polymorphism, Restriction Fragment Length Quantitative Trait, Heritable Quebec - epidemiology Regression Analysis Sex Distribution Systole - genetics |
| title | Genome-wide linkage analysis of systolic and diastolic blood pressure : The Québec Family Study |
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