common VLDLR polymorphism interacts with APOE genotype in the prediction of carotid artery disease risk
The genetic factors associated with carotid artery disease (CAAD) are not fully known. Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (...
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| Veröffentlicht in: | Journal of lipid research 2008-03, Vol.49 (3), p.588-596 |
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| creator | Crawford, Dana C Nord, Alex S Badzioch, Michael D Ranchalis, Jane McKinstry, Laura A Ahearn, Magdalena Bertucci, Caterina Shephard, Cynthia Wong, Michelle Rieder, Mark J Schellenberg, Gerard D Nickerson, Deborah A Heagerty, Patrick J Wijsman, Ellen M Jarvik, Gail P |
| description | The genetic factors associated with carotid artery disease (CAAD) are not fully known. Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLR was resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5' flanking region of VLDLR was associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR 1226 and APOE genotype for predicting CAAD case status. These findings may further our understanding of VLDLR function, its ligand APOE, and ultimately the pathogenesis of CAAD in the general population. |
| doi_str_mv | 10.1194/jlr.M700409-JLR200 |
| format | Article |
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Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLR was resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5' flanking region of VLDLR was associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR 1226 and APOE genotype for predicting CAAD case status. These findings may further our understanding of VLDLR function, its ligand APOE, and ultimately the pathogenesis of CAAD in the general population.</description><identifier>ISSN: 0022-2275</identifier><identifier>EISSN: 1539-7262</identifier><identifier>DOI: 10.1194/jlr.M700409-JLR200</identifier><identifier>PMID: 18056683</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>5' Flanking Region ; Apolipoproteins B ; Apolipoproteins E - genetics ; Body Mass Index ; Carotid Artery Diseases - genetics ; DNA Mutational Analysis ; Genetic Predisposition to Disease ; Genotype ; Humans ; Molecular Epidemiology ; Polymorphism, Single Nucleotide ; Receptors, LDL - genetics ; Risk Factors</subject><ispartof>Journal of lipid research, 2008-03, Vol.49 (3), p.588-596</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-3098f0c8c339640163d3f818b1dc2c2dc156514ec7a186e136de0f3abe9c03f53</citedby><cites>FETCH-LOGICAL-c394t-3098f0c8c339640163d3f818b1dc2c2dc156514ec7a186e136de0f3abe9c03f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3773,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18056683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crawford, Dana C</creatorcontrib><creatorcontrib>Nord, Alex S</creatorcontrib><creatorcontrib>Badzioch, Michael D</creatorcontrib><creatorcontrib>Ranchalis, Jane</creatorcontrib><creatorcontrib>McKinstry, Laura A</creatorcontrib><creatorcontrib>Ahearn, Magdalena</creatorcontrib><creatorcontrib>Bertucci, Caterina</creatorcontrib><creatorcontrib>Shephard, Cynthia</creatorcontrib><creatorcontrib>Wong, Michelle</creatorcontrib><creatorcontrib>Rieder, Mark J</creatorcontrib><creatorcontrib>Schellenberg, Gerard D</creatorcontrib><creatorcontrib>Nickerson, Deborah A</creatorcontrib><creatorcontrib>Heagerty, Patrick J</creatorcontrib><creatorcontrib>Wijsman, Ellen M</creatorcontrib><creatorcontrib>Jarvik, Gail P</creatorcontrib><title>common VLDLR polymorphism interacts with APOE genotype in the prediction of carotid artery disease risk</title><title>Journal of lipid research</title><addtitle>J Lipid Res</addtitle><description>The genetic factors associated with carotid artery disease (CAAD) are not fully known. Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLR was resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5' flanking region of VLDLR was associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR 1226 and APOE genotype for predicting CAAD case status. These findings may further our understanding of VLDLR function, its ligand APOE, and ultimately the pathogenesis of CAAD in the general population.</description><subject>5' Flanking Region</subject><subject>Apolipoproteins B</subject><subject>Apolipoproteins E - genetics</subject><subject>Body Mass Index</subject><subject>Carotid Artery Diseases - genetics</subject><subject>DNA Mutational Analysis</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Molecular Epidemiology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, LDL - genetics</subject><subject>Risk Factors</subject><issn>0022-2275</issn><issn>1539-7262</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1P3DAQhq2KCrZb_kAP4BO30Bk7cZwjAvqlVFS09Gp5ncmuIVkH26tq_31T7Uq9zBzmeV9pHsY-IFwjNuXH5yFef68BSmiKb-2jAHjDFljJpqiFEidsASBEIURdnbF3KT0DYFkqPGVnqKFSSssFW7swjmHLf7d37SOfwrAfQ5w2Po3cbzNF63Lif3ze8JsfD_d8TduQ9xPNR543xKdInXfZzw2h587GkH3HbZyTe975RDYRjz69vGdvezskOj_uJXv6dP_r9kvRPnz-envTFk42ZS4kNLoHp52UjSoBlexkr1GvsHPCic5hpSosydUWtSKUqiPopV1R40D2lVyyq0PvFMPrjlI2o0-OhsFuKeySqUEiqHkumTiALoaUIvVmin60cW8QzD-9ZtZrjnrNQe8cuji271Yjdf8jR58zcHkAehuMXc-fm6efAlAC6KrRspJ_AbwagOg</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Crawford, Dana C</creator><creator>Nord, Alex S</creator><creator>Badzioch, Michael D</creator><creator>Ranchalis, Jane</creator><creator>McKinstry, Laura A</creator><creator>Ahearn, Magdalena</creator><creator>Bertucci, Caterina</creator><creator>Shephard, Cynthia</creator><creator>Wong, Michelle</creator><creator>Rieder, Mark J</creator><creator>Schellenberg, Gerard D</creator><creator>Nickerson, Deborah A</creator><creator>Heagerty, Patrick J</creator><creator>Wijsman, Ellen M</creator><creator>Jarvik, Gail P</creator><general>American Society for Biochemistry and Molecular Biology</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>20080301</creationdate><title>common VLDLR polymorphism interacts with APOE genotype in the prediction of carotid artery disease risk</title><author>Crawford, Dana C ; 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Because of its role in lipid metabolism, we hypothesized that common genetic variation in the very low density lipoprotein receptor (VLDLR) gene is associated with severe CAAD (>80% stenosis), body mass index (BMI), and lipid traits in humans. VLDLR was resequenced for variation discovery in 92 subjects, and single nucleotide polymorphisms (tagSNPs) were chosen for genotyping in a larger cohort (n = 1,027). Of the 17 tagSNPs genotyped, one tagSNP (SNP 1226; rs1454626) located in the 5' flanking region of VLDLR was associated with CAAD, BMI, and LDL-associated apolipoprotein B (apoB). We also identified receptor-ligand genetic interactions between VLDLR 1226 and APOE genotype for predicting CAAD case status. 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| source | American Society for Biochemistry and Molecular Biology; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | 5' Flanking Region Apolipoproteins B Apolipoproteins E - genetics Body Mass Index Carotid Artery Diseases - genetics DNA Mutational Analysis Genetic Predisposition to Disease Genotype Humans Molecular Epidemiology Polymorphism, Single Nucleotide Receptors, LDL - genetics Risk Factors |
| title | common VLDLR polymorphism interacts with APOE genotype in the prediction of carotid artery disease risk |
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