Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis
Objective: Interaction of advanced glycation end products (AGEs) with their receptors (RAGE) plays an important role in inflammation in auto-immune diseases. Several functional polymorphisms of RAGE have been described. In this study we analysed the role of RAGE polymorphisms in disease susceptibili...
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| Veröffentlicht in: | Lupus 2012-08, Vol.21 (9), p.959-968 |
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| creator | Martens, HA Nienhuis, HLA Gross, S der Steege, G van Brouwer, E Berden, JHM Sévaux, RGL de Derksen, RHWM Voskuyl, AE Berger, SP Navis, GJ Nolte, IM Kallenberg, CGM Bijl, M |
| description | Objective: Interaction of advanced glycation end products (AGEs) with their receptors (RAGE) plays an important role in inflammation in auto-immune diseases. Several functional polymorphisms of RAGE have been described. In this study we analysed the role of RAGE polymorphisms in disease susceptibility for systemic lupus erythematosus (SLE). In addition, we investigated whether these polymorphisms in SLE are associated with serum levels of soluble RAGE (sRAGE), renal involvement (lupus nephritis (LN)) and its outcome. Methods: For this cross-sectional study DNA samples of 97 SLE patients, 114 LN patients and 429 healthy controls (HC) were genotyped for four RAGE polymorphisms: −429 T/C, −374 T/A, 2184 A/G and Gly82Ser. Differences in genotype frequencies and allele frequencies were tested between patients and HCs. In SLE patients, sRAGE was measured by enzyme-linked immunosorbent assay (ELISA). In addition, association of genotypes with sRAGE and disease severity in LN was analysed. Results: The C allele of −429 T/C, the T allele of −374 T/A and the G allele of 2184 A/G were significantly more prevalent in SLE and LN compared with HC. In LN, the C allele of RAGE −429 T/C, the A allele of −374 T/A and the G allele of RAGE 2184 A/G polymorphism were significantly associated with more proteinuria and worse renal function during the first two years of treatment. No association of genotype with sRAGE was found. Conclusion: RAGE polymorphisms are associated with susceptibility to SLE and LN. In addition, some of these polymorphisms are likely to be associated with disease severity and initial response to treatment in LN. |
| doi_str_mv | 10.1177/0961203312444495 |
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Several functional polymorphisms of RAGE have been described. In this study we analysed the role of RAGE polymorphisms in disease susceptibility for systemic lupus erythematosus (SLE). In addition, we investigated whether these polymorphisms in SLE are associated with serum levels of soluble RAGE (sRAGE), renal involvement (lupus nephritis (LN)) and its outcome. Methods: For this cross-sectional study DNA samples of 97 SLE patients, 114 LN patients and 429 healthy controls (HC) were genotyped for four RAGE polymorphisms: −429 T/C, −374 T/A, 2184 A/G and Gly82Ser. Differences in genotype frequencies and allele frequencies were tested between patients and HCs. In SLE patients, sRAGE was measured by enzyme-linked immunosorbent assay (ELISA). In addition, association of genotypes with sRAGE and disease severity in LN was analysed. Results: The C allele of −429 T/C, the T allele of −374 T/A and the G allele of 2184 A/G were significantly more prevalent in SLE and LN compared with HC. In LN, the C allele of RAGE −429 T/C, the A allele of −374 T/A and the G allele of RAGE 2184 A/G polymorphism were significantly associated with more proteinuria and worse renal function during the first two years of treatment. No association of genotype with sRAGE was found. Conclusion: RAGE polymorphisms are associated with susceptibility to SLE and LN. In addition, some of these polymorphisms are likely to be associated with disease severity and initial response to treatment in LN.</description><identifier>ISSN: 0961-2033</identifier><identifier>EISSN: 1477-0962</identifier><identifier>DOI: 10.1177/0961203312444495</identifier><identifier>PMID: 22513366</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Advanced glycosylation end products ; Aged ; Alzheimer's disease ; Atherosclerosis ; Cardiovascular disease ; Cross-Sectional Studies ; Enzyme-linked immunosorbent assay ; Female ; Gene frequency ; Gene polymorphism ; Genetic Predisposition to Disease ; Genotype ; Humans ; Immunology ; Inflammation ; Kidney diseases ; Linkage Disequilibrium ; Lupus ; Lupus Erythematosus, Systemic - genetics ; Lupus nephritis ; Lupus Nephritis - genetics ; Male ; Middle Aged ; Nephrology ; Polymorphism ; Polymorphism, Genetic ; Proteinuria ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - genetics ; Renal function ; Rheumatology ; Serum levels ; Systemic lupus erythematosus</subject><ispartof>Lupus, 2012-08, Vol.21 (9), p.959-968</ispartof><rights>The Author(s), 2012. Reprints and permissions: http://www.sagepub.co.uk/journalsPermissions.nav</rights><rights>SAGE Publications © Aug 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-5694368bb7dae7b5b8cf158fd555ade9f0d69b05465154f9457c0ea027736f623</citedby><cites>FETCH-LOGICAL-c398t-5694368bb7dae7b5b8cf158fd555ade9f0d69b05465154f9457c0ea027736f623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0961203312444495$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0961203312444495$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21818,27923,27924,43620,43621</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22513366$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martens, HA</creatorcontrib><creatorcontrib>Nienhuis, HLA</creatorcontrib><creatorcontrib>Gross, S</creatorcontrib><creatorcontrib>der Steege, G van</creatorcontrib><creatorcontrib>Brouwer, E</creatorcontrib><creatorcontrib>Berden, JHM</creatorcontrib><creatorcontrib>Sévaux, RGL de</creatorcontrib><creatorcontrib>Derksen, RHWM</creatorcontrib><creatorcontrib>Voskuyl, AE</creatorcontrib><creatorcontrib>Berger, SP</creatorcontrib><creatorcontrib>Navis, GJ</creatorcontrib><creatorcontrib>Nolte, IM</creatorcontrib><creatorcontrib>Kallenberg, CGM</creatorcontrib><creatorcontrib>Bijl, M</creatorcontrib><title>Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis</title><title>Lupus</title><addtitle>Lupus</addtitle><description>Objective: Interaction of advanced glycation end products (AGEs) with their receptors (RAGE) plays an important role in inflammation in auto-immune diseases. Several functional polymorphisms of RAGE have been described. In this study we analysed the role of RAGE polymorphisms in disease susceptibility for systemic lupus erythematosus (SLE). In addition, we investigated whether these polymorphisms in SLE are associated with serum levels of soluble RAGE (sRAGE), renal involvement (lupus nephritis (LN)) and its outcome. Methods: For this cross-sectional study DNA samples of 97 SLE patients, 114 LN patients and 429 healthy controls (HC) were genotyped for four RAGE polymorphisms: −429 T/C, −374 T/A, 2184 A/G and Gly82Ser. Differences in genotype frequencies and allele frequencies were tested between patients and HCs. In SLE patients, sRAGE was measured by enzyme-linked immunosorbent assay (ELISA). In addition, association of genotypes with sRAGE and disease severity in LN was analysed. Results: The C allele of −429 T/C, the T allele of −374 T/A and the G allele of 2184 A/G were significantly more prevalent in SLE and LN compared with HC. In LN, the C allele of RAGE −429 T/C, the A allele of −374 T/A and the G allele of RAGE 2184 A/G polymorphism were significantly associated with more proteinuria and worse renal function during the first two years of treatment. No association of genotype with sRAGE was found. Conclusion: RAGE polymorphisms are associated with susceptibility to SLE and LN. In addition, some of these polymorphisms are likely to be associated with disease severity and initial response to treatment in LN.</description><subject>Adult</subject><subject>Advanced glycosylation end products</subject><subject>Aged</subject><subject>Alzheimer's disease</subject><subject>Atherosclerosis</subject><subject>Cardiovascular disease</subject><subject>Cross-Sectional Studies</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Gene frequency</subject><subject>Gene polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Linkage Disequilibrium</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - genetics</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Nephrology</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Proteinuria</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - genetics</subject><subject>Renal function</subject><subject>Rheumatology</subject><subject>Serum levels</subject><subject>Systemic lupus erythematosus</subject><issn>0961-2033</issn><issn>1477-0962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkVFrFTEQhYMo9rb67pMEfGkfVpPNJtk8llKrUBCKPl-yyWxvyu5mzWQr-1f8teZyryIFwUAImfnOGYZDyBvO3nOu9QdmFK-ZELxuyjHyGdnwRuuq1OvnZLNvV_v-CTlFfGCMCW7US3JS15ILodSG_LwDB3OOifblWv9oJwee3g-rsznEicLk6ZyiX1xGen53eXN9Qec4rGNM8y7giNQmoBYxumBzkf4IeUdxxQxjcHRY5gUppDXvYLQ5YvnZYukDgkWgCI-QQl5pmI7sBPOuVAK-Ii96OyC8Pr5n5NvH669Xn6rbLzefry5vKydMmyupTCNU23XaW9Cd7FrXc9n2XkppPZieeWU6JhsluWx600jtGFhWay1Ur2pxRs4PvmXN7wtg3o4BHQyDnSAuuOWszGlNo9v_QevWCMVkQd89QR_ikqayyJ5itZSiaQrFDpRLETFBv51TGG1aC7TdR7x9GnGRvD0aL90I_o_gd6YFqA4A2nv4e-o_DH8B-WKvzA</recordid><startdate>201208</startdate><enddate>201208</enddate><creator>Martens, HA</creator><creator>Nienhuis, HLA</creator><creator>Gross, S</creator><creator>der Steege, G van</creator><creator>Brouwer, E</creator><creator>Berden, JHM</creator><creator>Sévaux, RGL de</creator><creator>Derksen, RHWM</creator><creator>Voskuyl, AE</creator><creator>Berger, SP</creator><creator>Navis, GJ</creator><creator>Nolte, IM</creator><creator>Kallenberg, CGM</creator><creator>Bijl, M</creator><general>SAGE Publications</general><general>Sage Publications 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>3V.</scope><scope>7T5</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>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>201208</creationdate><title>Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis</title><author>Martens, HA ; Nienhuis, HLA ; Gross, S ; der Steege, G van ; Brouwer, E ; Berden, JHM ; Sévaux, RGL de ; Derksen, RHWM ; Voskuyl, AE ; Berger, SP ; Navis, GJ ; Nolte, IM ; Kallenberg, CGM ; Bijl, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-5694368bb7dae7b5b8cf158fd555ade9f0d69b05465154f9457c0ea027736f623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Advanced glycosylation end products</topic><topic>Aged</topic><topic>Alzheimer's disease</topic><topic>Atherosclerosis</topic><topic>Cardiovascular disease</topic><topic>Cross-Sectional Studies</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Gene frequency</topic><topic>Gene polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Kidney diseases</topic><topic>Linkage Disequilibrium</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - genetics</topic><topic>Lupus nephritis</topic><topic>Lupus Nephritis - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Nephrology</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Proteinuria</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - genetics</topic><topic>Renal function</topic><topic>Rheumatology</topic><topic>Serum levels</topic><topic>Systemic lupus erythematosus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martens, HA</creatorcontrib><creatorcontrib>Nienhuis, HLA</creatorcontrib><creatorcontrib>Gross, S</creatorcontrib><creatorcontrib>der Steege, G van</creatorcontrib><creatorcontrib>Brouwer, E</creatorcontrib><creatorcontrib>Berden, JHM</creatorcontrib><creatorcontrib>Sévaux, RGL de</creatorcontrib><creatorcontrib>Derksen, RHWM</creatorcontrib><creatorcontrib>Voskuyl, AE</creatorcontrib><creatorcontrib>Berger, SP</creatorcontrib><creatorcontrib>Navis, GJ</creatorcontrib><creatorcontrib>Nolte, IM</creatorcontrib><creatorcontrib>Kallenberg, CGM</creatorcontrib><creatorcontrib>Bijl, M</creatorcontrib><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>Immunology Abstracts</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 Essentials</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>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Lupus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martens, HA</au><au>Nienhuis, HLA</au><au>Gross, S</au><au>der Steege, G van</au><au>Brouwer, E</au><au>Berden, JHM</au><au>Sévaux, RGL de</au><au>Derksen, RHWM</au><au>Voskuyl, AE</au><au>Berger, SP</au><au>Navis, GJ</au><au>Nolte, IM</au><au>Kallenberg, CGM</au><au>Bijl, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis</atitle><jtitle>Lupus</jtitle><addtitle>Lupus</addtitle><date>2012-08</date><risdate>2012</risdate><volume>21</volume><issue>9</issue><spage>959</spage><epage>968</epage><pages>959-968</pages><issn>0961-2033</issn><eissn>1477-0962</eissn><abstract>Objective: Interaction of advanced glycation end products (AGEs) with their receptors (RAGE) plays an important role in inflammation in auto-immune diseases. Several functional polymorphisms of RAGE have been described. In this study we analysed the role of RAGE polymorphisms in disease susceptibility for systemic lupus erythematosus (SLE). In addition, we investigated whether these polymorphisms in SLE are associated with serum levels of soluble RAGE (sRAGE), renal involvement (lupus nephritis (LN)) and its outcome. Methods: For this cross-sectional study DNA samples of 97 SLE patients, 114 LN patients and 429 healthy controls (HC) were genotyped for four RAGE polymorphisms: −429 T/C, −374 T/A, 2184 A/G and Gly82Ser. Differences in genotype frequencies and allele frequencies were tested between patients and HCs. In SLE patients, sRAGE was measured by enzyme-linked immunosorbent assay (ELISA). In addition, association of genotypes with sRAGE and disease severity in LN was analysed. Results: The C allele of −429 T/C, the T allele of −374 T/A and the G allele of 2184 A/G were significantly more prevalent in SLE and LN compared with HC. In LN, the C allele of RAGE −429 T/C, the A allele of −374 T/A and the G allele of RAGE 2184 A/G polymorphism were significantly associated with more proteinuria and worse renal function during the first two years of treatment. No association of genotype with sRAGE was found. Conclusion: RAGE polymorphisms are associated with susceptibility to SLE and LN. In addition, some of these polymorphisms are likely to be associated with disease severity and initial response to treatment in LN.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>22513366</pmid><doi>10.1177/0961203312444495</doi><tpages>10</tpages></addata></record> |
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| ispartof | Lupus, 2012-08, Vol.21 (9), p.959-968 |
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| subjects | Adult Advanced glycosylation end products Aged Alzheimer's disease Atherosclerosis Cardiovascular disease Cross-Sectional Studies Enzyme-linked immunosorbent assay Female Gene frequency Gene polymorphism Genetic Predisposition to Disease Genotype Humans Immunology Inflammation Kidney diseases Linkage Disequilibrium Lupus Lupus Erythematosus, Systemic - genetics Lupus nephritis Lupus Nephritis - genetics Male Middle Aged Nephrology Polymorphism Polymorphism, Genetic Proteinuria Receptor for Advanced Glycation End Products Receptors, Immunologic - genetics Renal function Rheumatology Serum levels Systemic lupus erythematosus |
| title | Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis |
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