Variants in ALOX5 , ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: The Athero-Express Genomics Study
Abstract Background The eicosanoid genes ALOX5 , ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods We included patients from the Stockholm...
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| Veröffentlicht in: | Atherosclerosis 2015-04, Vol.239 (2), p.528-538 |
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| creator | van der Laan, Sander W Foroughi Asl, Hassan van den Borne, Pleunie van Setten, Jessica van der Perk, M.E. Madeleine van de Weg, Sander M Schoneveld, Arjan H de Kleijn, Dominique P.V Michoel, Tom Björkegren, Johan L.M den Ruijter, Hester M Asselbergs, Folkert W de Bakker, Paul I.W Pasterkamp, Gerard |
| description | Abstract Background The eicosanoid genes ALOX5 , ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods We included patients from the Stockholm Atherosclerosis Gene Expression study (STAGE, N = 109), and the Athero-Express Biobank Study (AE, N = 1443). We tested 1453 single-nucleotide variants (SNVs) in ALOX5 , ALOX5AP and LTA4H for association with gene expression in STAGE. We also tested these SNVs for association with seven histologically defined plaque phenotypes in the AE (which included calcification, collagen, cellular content, atheroma size, and intraplaque vessel density and hemorrhage). Results We replicate a known cis -eQTL (rs6538697, p = 1.96 × 10−6 ) for LTA4H expression in whole blood of patients from STAGE. We found no significant association for any of the SNVs tested with serum levels of ALOX5 or ALOX5AP (p > 5.79 × 10−4 ). For atherosclerotic plaque phenotypes the strongest associations were found for intraplaque vessel density and smooth muscle cells in the ALOX5AP locus (p > 1.67 × 10−4 ). Conclusions We replicate a known eQTL for LTA4H expression in whole blood using STAGE data. We found no associations of variants in and around ALOX5 , ALOX5AP and LTA4H with serum ALOX5 or ALOX5AP levels, or plaque phenotypes. On the supposition that these genes play a causal role in atherosclerosis, these results suggest that common variants in these loci play a limited role (if any) in influencing advanced atherosclerotic plaque morphology to the extent that it impacts atherosclerotic disease. |
| doi_str_mv | 10.1016/j.atherosclerosis.2015.01.018 |
| format | Article |
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Madeleine ; van de Weg, Sander M ; Schoneveld, Arjan H ; de Kleijn, Dominique P.V ; Michoel, Tom ; Björkegren, Johan L.M ; den Ruijter, Hester M ; Asselbergs, Folkert W ; de Bakker, Paul I.W ; Pasterkamp, Gerard</creator><creatorcontrib>van der Laan, Sander W ; Foroughi Asl, Hassan ; van den Borne, Pleunie ; van Setten, Jessica ; van der Perk, M.E. Madeleine ; van de Weg, Sander M ; Schoneveld, Arjan H ; de Kleijn, Dominique P.V ; Michoel, Tom ; Björkegren, Johan L.M ; den Ruijter, Hester M ; Asselbergs, Folkert W ; de Bakker, Paul I.W ; Pasterkamp, Gerard</creatorcontrib><description>Abstract Background The eicosanoid genes ALOX5 , ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods We included patients from the Stockholm Atherosclerosis Gene Expression study (STAGE, N = 109), and the Athero-Express Biobank Study (AE, N = 1443). We tested 1453 single-nucleotide variants (SNVs) in ALOX5 , ALOX5AP and LTA4H for association with gene expression in STAGE. We also tested these SNVs for association with seven histologically defined plaque phenotypes in the AE (which included calcification, collagen, cellular content, atheroma size, and intraplaque vessel density and hemorrhage). Results We replicate a known cis -eQTL (rs6538697, p = 1.96 × 10−6 ) for LTA4H expression in whole blood of patients from STAGE. We found no significant association for any of the SNVs tested with serum levels of ALOX5 or ALOX5AP (p > 5.79 × 10−4 ). For atherosclerotic plaque phenotypes the strongest associations were found for intraplaque vessel density and smooth muscle cells in the ALOX5AP locus (p > 1.67 × 10−4 ). Conclusions We replicate a known eQTL for LTA4H expression in whole blood using STAGE data. We found no associations of variants in and around ALOX5 , ALOX5AP and LTA4H with serum ALOX5 or ALOX5AP levels, or plaque phenotypes. On the supposition that these genes play a causal role in atherosclerosis, these results suggest that common variants in these loci play a limited role (if any) in influencing advanced atherosclerotic plaque morphology to the extent that it impacts atherosclerotic disease.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2015.01.018</identifier><identifier>PMID: 25721704</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>5-Lipoxygenase-Activating Proteins - genetics ; Aged ; ALOX5 ; Arachidonate 5-Lipoxygenase - genetics ; Atherosclerosis ; Atherosclerosis - diagnosis ; Atherosclerosis - enzymology ; Atherosclerosis - genetics ; Biological Specimen Banks ; Cardiovascular ; Carotid Artery Diseases - diagnosis ; Carotid Artery Diseases - enzymology ; Carotid Artery Diseases - genetics ; Coronary Artery Disease - diagnosis ; Coronary Artery Disease - enzymology ; Coronary Artery Disease - genetics ; Eicosanoids ; Epoxide Hydrolases - genetics ; Female ; Femoral Artery - enzymology ; Femoral Artery - pathology ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genomics - methods ; Humans ; Male ; Middle Aged ; Netherlands ; Phenotype ; Plaque ; Plaque, Atherosclerotic ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; Single-nucleotide polymorphism ; Sweden</subject><ispartof>Atherosclerosis, 2015-04, Vol.239 (2), p.528-538</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2015 Elsevier Ireland Ltd</rights><rights>Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-ffb781d02ac42844df6c6b3f9823f79e59ba7125cae9d615fb48fbf69128dc623</citedby><cites>FETCH-LOGICAL-c482t-ffb781d02ac42844df6c6b3f9823f79e59ba7125cae9d615fb48fbf69128dc623</cites><orcidid>0000-0001-6888-1404</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.atherosclerosis.2015.01.018$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25721704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:130895592$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Laan, Sander W</creatorcontrib><creatorcontrib>Foroughi Asl, Hassan</creatorcontrib><creatorcontrib>van den Borne, Pleunie</creatorcontrib><creatorcontrib>van Setten, Jessica</creatorcontrib><creatorcontrib>van der Perk, M.E. Madeleine</creatorcontrib><creatorcontrib>van de Weg, Sander M</creatorcontrib><creatorcontrib>Schoneveld, Arjan H</creatorcontrib><creatorcontrib>de Kleijn, Dominique P.V</creatorcontrib><creatorcontrib>Michoel, Tom</creatorcontrib><creatorcontrib>Björkegren, Johan L.M</creatorcontrib><creatorcontrib>den Ruijter, Hester M</creatorcontrib><creatorcontrib>Asselbergs, Folkert W</creatorcontrib><creatorcontrib>de Bakker, Paul I.W</creatorcontrib><creatorcontrib>Pasterkamp, Gerard</creatorcontrib><title>Variants in ALOX5 , ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: The Athero-Express Genomics Study</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract Background The eicosanoid genes ALOX5 , ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods We included patients from the Stockholm Atherosclerosis Gene Expression study (STAGE, N = 109), and the Athero-Express Biobank Study (AE, N = 1443). We tested 1453 single-nucleotide variants (SNVs) in ALOX5 , ALOX5AP and LTA4H for association with gene expression in STAGE. We also tested these SNVs for association with seven histologically defined plaque phenotypes in the AE (which included calcification, collagen, cellular content, atheroma size, and intraplaque vessel density and hemorrhage). Results We replicate a known cis -eQTL (rs6538697, p = 1.96 × 10−6 ) for LTA4H expression in whole blood of patients from STAGE. We found no significant association for any of the SNVs tested with serum levels of ALOX5 or ALOX5AP (p > 5.79 × 10−4 ). For atherosclerotic plaque phenotypes the strongest associations were found for intraplaque vessel density and smooth muscle cells in the ALOX5AP locus (p > 1.67 × 10−4 ). Conclusions We replicate a known eQTL for LTA4H expression in whole blood using STAGE data. We found no associations of variants in and around ALOX5 , ALOX5AP and LTA4H with serum ALOX5 or ALOX5AP levels, or plaque phenotypes. On the supposition that these genes play a causal role in atherosclerosis, these results suggest that common variants in these loci play a limited role (if any) in influencing advanced atherosclerotic plaque morphology to the extent that it impacts atherosclerotic disease.</description><subject>5-Lipoxygenase-Activating Proteins - genetics</subject><subject>Aged</subject><subject>ALOX5</subject><subject>Arachidonate 5-Lipoxygenase - genetics</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - diagnosis</subject><subject>Atherosclerosis - enzymology</subject><subject>Atherosclerosis - genetics</subject><subject>Biological Specimen Banks</subject><subject>Cardiovascular</subject><subject>Carotid Artery Diseases - diagnosis</subject><subject>Carotid Artery Diseases - enzymology</subject><subject>Carotid Artery Diseases - genetics</subject><subject>Coronary Artery Disease - diagnosis</subject><subject>Coronary Artery Disease - enzymology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Eicosanoids</subject><subject>Epoxide Hydrolases - genetics</subject><subject>Female</subject><subject>Femoral Artery - enzymology</subject><subject>Femoral Artery - pathology</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-Wide Association Study</subject><subject>Genomics - methods</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Netherlands</subject><subject>Phenotype</subject><subject>Plaque</subject><subject>Plaque, Atherosclerotic</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Quantitative Trait Loci</subject><subject>Single-nucleotide polymorphism</subject><subject>Sweden</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNklGL1DAQx4Mo3nr6FSQvgg92TbJJmwoK5Tj3hIUTbhXfQppM2ex125qknvvqJze16yH3JAyZkPxmJpn_IPSKkiUlNH-7X-q4A98H006rC0tGqFgSmkw-QgsqizKjXPLHaEEIo1lJBTlDz0LYE0J4QeVTdMZEwWhB-AL9-qq9010M2HW42lx_E_jN7KvPWHcWb7YVv8LaA-76iHUIvXE6gsV3Lu7wv2-JzuCh1d9HwMMOEn0cILzD2x3g6g-WXf4cPISA1-n24EzAN3G0x-foSaPbAC9O_hx9-Xi5vbjKNtfrTxfVJjNcspg1TV1IagnThjPJuW1yk9erppRs1RQliLLWBWXCaChtTkVTc9nUTV5SJq3J2eocZXPecAfDWKvBu4P2R9Vrp05Ht2kHSlCxkhP_euYH36dPhagOLhhoW91BPwZF85wzkpdCJPT9jJrUjOChuU9OiZpkU3v1QDY1yaYITSZT_MtTqbE-gL2P_qtTAtYzAKlBPxx4FYyDzoB1HkxUtnf_XerDg0ymdZ0zur2FI4R9P_ouqaCoCkwRdTPN0DRCyQgRjKx-A3DPyKc</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>van der Laan, Sander W</creator><creator>Foroughi Asl, Hassan</creator><creator>van den Borne, Pleunie</creator><creator>van Setten, Jessica</creator><creator>van der Perk, M.E. Madeleine</creator><creator>van de Weg, Sander M</creator><creator>Schoneveld, Arjan H</creator><creator>de Kleijn, Dominique P.V</creator><creator>Michoel, Tom</creator><creator>Björkegren, Johan L.M</creator><creator>den Ruijter, Hester M</creator><creator>Asselbergs, Folkert W</creator><creator>de Bakker, Paul I.W</creator><creator>Pasterkamp, Gerard</creator><general>Elsevier Ireland Ltd</general><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><scope>ADTPV</scope><scope>AOWAS</scope><orcidid>https://orcid.org/0000-0001-6888-1404</orcidid></search><sort><creationdate>20150401</creationdate><title>Variants in ALOX5 , ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: The Athero-Express Genomics Study</title><author>van der Laan, Sander W ; Foroughi Asl, Hassan ; van den Borne, Pleunie ; van Setten, Jessica ; van der Perk, M.E. Madeleine ; van de Weg, Sander M ; Schoneveld, Arjan H ; de Kleijn, Dominique P.V ; Michoel, Tom ; Björkegren, Johan L.M ; den Ruijter, Hester M ; Asselbergs, Folkert W ; de Bakker, Paul I.W ; Pasterkamp, Gerard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-ffb781d02ac42844df6c6b3f9823f79e59ba7125cae9d615fb48fbf69128dc623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>5-Lipoxygenase-Activating Proteins - genetics</topic><topic>Aged</topic><topic>ALOX5</topic><topic>Arachidonate 5-Lipoxygenase - genetics</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - diagnosis</topic><topic>Atherosclerosis - enzymology</topic><topic>Atherosclerosis - genetics</topic><topic>Biological Specimen Banks</topic><topic>Cardiovascular</topic><topic>Carotid Artery Diseases - diagnosis</topic><topic>Carotid Artery Diseases - enzymology</topic><topic>Carotid Artery Diseases - genetics</topic><topic>Coronary Artery Disease - diagnosis</topic><topic>Coronary Artery Disease - enzymology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Eicosanoids</topic><topic>Epoxide Hydrolases - genetics</topic><topic>Female</topic><topic>Femoral Artery - enzymology</topic><topic>Femoral Artery - pathology</topic><topic>Genetic Predisposition to Disease</topic><topic>Genome-Wide Association Study</topic><topic>Genomics - methods</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Netherlands</topic><topic>Phenotype</topic><topic>Plaque</topic><topic>Plaque, Atherosclerotic</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Quantitative Trait Loci</topic><topic>Single-nucleotide polymorphism</topic><topic>Sweden</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van der Laan, Sander W</creatorcontrib><creatorcontrib>Foroughi Asl, Hassan</creatorcontrib><creatorcontrib>van den Borne, Pleunie</creatorcontrib><creatorcontrib>van Setten, Jessica</creatorcontrib><creatorcontrib>van der Perk, M.E. Madeleine</creatorcontrib><creatorcontrib>van de Weg, Sander M</creatorcontrib><creatorcontrib>Schoneveld, Arjan H</creatorcontrib><creatorcontrib>de Kleijn, Dominique P.V</creatorcontrib><creatorcontrib>Michoel, Tom</creatorcontrib><creatorcontrib>Björkegren, Johan L.M</creatorcontrib><creatorcontrib>den Ruijter, Hester M</creatorcontrib><creatorcontrib>Asselbergs, Folkert W</creatorcontrib><creatorcontrib>de Bakker, Paul I.W</creatorcontrib><creatorcontrib>Pasterkamp, Gerard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Laan, Sander W</au><au>Foroughi Asl, Hassan</au><au>van den Borne, Pleunie</au><au>van Setten, Jessica</au><au>van der Perk, M.E. Madeleine</au><au>van de Weg, Sander M</au><au>Schoneveld, Arjan H</au><au>de Kleijn, Dominique P.V</au><au>Michoel, Tom</au><au>Björkegren, Johan L.M</au><au>den Ruijter, Hester M</au><au>Asselbergs, Folkert W</au><au>de Bakker, Paul I.W</au><au>Pasterkamp, Gerard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variants in ALOX5 , ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: The Athero-Express Genomics Study</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>239</volume><issue>2</issue><spage>528</spage><epage>538</epage><pages>528-538</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Background The eicosanoid genes ALOX5 , ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods We included patients from the Stockholm Atherosclerosis Gene Expression study (STAGE, N = 109), and the Athero-Express Biobank Study (AE, N = 1443). We tested 1453 single-nucleotide variants (SNVs) in ALOX5 , ALOX5AP and LTA4H for association with gene expression in STAGE. We also tested these SNVs for association with seven histologically defined plaque phenotypes in the AE (which included calcification, collagen, cellular content, atheroma size, and intraplaque vessel density and hemorrhage). Results We replicate a known cis -eQTL (rs6538697, p = 1.96 × 10−6 ) for LTA4H expression in whole blood of patients from STAGE. We found no significant association for any of the SNVs tested with serum levels of ALOX5 or ALOX5AP (p > 5.79 × 10−4 ). For atherosclerotic plaque phenotypes the strongest associations were found for intraplaque vessel density and smooth muscle cells in the ALOX5AP locus (p > 1.67 × 10−4 ). Conclusions We replicate a known eQTL for LTA4H expression in whole blood using STAGE data. We found no associations of variants in and around ALOX5 , ALOX5AP and LTA4H with serum ALOX5 or ALOX5AP levels, or plaque phenotypes. On the supposition that these genes play a causal role in atherosclerosis, these results suggest that common variants in these loci play a limited role (if any) in influencing advanced atherosclerotic plaque morphology to the extent that it impacts atherosclerotic disease.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>25721704</pmid><doi>10.1016/j.atherosclerosis.2015.01.018</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-6888-1404</orcidid></addata></record> |
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| ispartof | Atherosclerosis, 2015-04, Vol.239 (2), p.528-538 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 5-Lipoxygenase-Activating Proteins - genetics Aged ALOX5 Arachidonate 5-Lipoxygenase - genetics Atherosclerosis Atherosclerosis - diagnosis Atherosclerosis - enzymology Atherosclerosis - genetics Biological Specimen Banks Cardiovascular Carotid Artery Diseases - diagnosis Carotid Artery Diseases - enzymology Carotid Artery Diseases - genetics Coronary Artery Disease - diagnosis Coronary Artery Disease - enzymology Coronary Artery Disease - genetics Eicosanoids Epoxide Hydrolases - genetics Female Femoral Artery - enzymology Femoral Artery - pathology Genetic Predisposition to Disease Genome-Wide Association Study Genomics - methods Humans Male Middle Aged Netherlands Phenotype Plaque Plaque, Atherosclerotic Polymorphism, Single Nucleotide Quantitative Trait Loci Single-nucleotide polymorphism Sweden |
| title | Variants in ALOX5 , ALOX5AP and LTA4H are not associated with atherosclerotic plaque phenotypes: The Athero-Express Genomics Study |
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