A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis
Objectives The severity of joint destruction is highly variable between rheumatoid arthritis (RA) patients. The majority of its heritability is still unexplained. Several autoimmune diseases share genetic risk variants that may also influence disease progression. We aimed to identify genetic risk fa...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2014-06, Vol.73 (6), p.1163-1169 |
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| creator | de Rooy, D P C Zhernakova, A Tsonaka, R Willemze, A Kurreeman, B A S Trynka, G van Toorn, L Toes, R E M Huizinga, T W J Houwing-Duistermaat, J J Gregersen, P K van der Helm-van Mil, A H M |
| description | Objectives The severity of joint destruction is highly variable between rheumatoid arthritis (RA) patients. The majority of its heritability is still unexplained. Several autoimmune diseases share genetic risk variants that may also influence disease progression. We aimed to identify genetic risk factors for the severity of joint damage in RA by studying genetic susceptibility loci of several autoimmune diseases. Methods In phase 1, 3143 sets of x-rays of 646 Dutch RA patients taken over 7 years (Sharp van der Heijde (SHS) scored) were studied. Genotyping was done by Immunochip. Associations of single-nucleotide polymorphisms (SNPs) with minor allele frequency (MAF) >0.01 and joint destruction were analysed. In phase 2, 686 North American RA patients with 926 SHS-scored x-rays over 15 years of follow-up were evaluated. In both phases multiple testing corrections were done for the number of uncorrelated SNPs; the thresholds for significance were p |
| doi_str_mv | 10.1136/annrheumdis-2013-203375 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1521325548</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4008666721</sourcerecordid><originalsourceid>FETCH-LOGICAL-b384t-58f1d03e8d93fcf39d981f3b94605567e48e5b2e59b53dd7253b10b935f1cd0c3</originalsourceid><addsrcrecordid>eNqNkUFv1DAQhS0EokvhL4AlLlwCdia242NVFYrUCg5wtpx4sutVYhfbacWNn46XXRDixGVGo_ne05MeIa84e8s5yHc2hLTDdXE-Ny3jUAeAEo_Ihneyr5dkj8mGMQZNp6U6I89y3teT9bx_Ss5akFpKYBvy44JuMWDxI723ydtQqA-07JAm3PoYaJzo7e3nRlOfqc05jt4WdPTBlx3NmNaFzniPc30GR-9S3CbM-STcR1_9nF3sFg-2vyLbEr2jNpVd8sXn5-TJZOeML077nHx9f_Xl8rq5-fTh4-XFTTNA35VG9BN3DLB3GqZxAu10zycYdCeZEFJh16MYWhR6EOCcagUMnA0axMRHx0Y4J2-OvjXjtxVzMYvPI86zDRjXbLhoObRCdH1FX_-D7uOaQk1nuFJKM9UpqJQ6UmOKOSeczF3yi03fDWfmUJL5qyRzKMkcS6rKlyf_dVjQ_dH9bqUC7REYlv1_u_4E1NyhxQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1777907473</pqid></control><display><type>article</type><title>A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><creator>de Rooy, D P C ; Zhernakova, A ; Tsonaka, R ; Willemze, A ; Kurreeman, B A S ; Trynka, G ; van Toorn, L ; Toes, R E M ; Huizinga, T W J ; Houwing-Duistermaat, J J ; Gregersen, P K ; van der Helm-van Mil, A H M</creator><creatorcontrib>de Rooy, D P C ; Zhernakova, A ; Tsonaka, R ; Willemze, A ; Kurreeman, B A S ; Trynka, G ; van Toorn, L ; Toes, R E M ; Huizinga, T W J ; Houwing-Duistermaat, J J ; Gregersen, P K ; van der Helm-van Mil, A H M</creatorcontrib><description>Objectives The severity of joint destruction is highly variable between rheumatoid arthritis (RA) patients. The majority of its heritability is still unexplained. Several autoimmune diseases share genetic risk variants that may also influence disease progression. We aimed to identify genetic risk factors for the severity of joint damage in RA by studying genetic susceptibility loci of several autoimmune diseases. Methods In phase 1, 3143 sets of x-rays of 646 Dutch RA patients taken over 7 years (Sharp van der Heijde (SHS) scored) were studied. Genotyping was done by Immunochip. Associations of single-nucleotide polymorphisms (SNPs) with minor allele frequency (MAF) >0.01 and joint destruction were analysed. In phase 2, 686 North American RA patients with 926 SHS-scored x-rays over 15 years of follow-up were evaluated. In both phases multiple testing corrections were done for the number of uncorrelated SNPs; the thresholds for significance were p<1.1×10−6 and p<0.0036. Matrix metalloproteinase 9 (MMP-9) levels were measured with ELISA in baseline serum samples. Results In phase 1, 109 SNPs associated significantly with joint destruction (p<1.1×10−6). Of these, 76 were located in the HLA region; the 33 non-HLA variants were studied in phase 2. Here two variants were associated with the severity of joint destruction: rs451066 on chromosome 14 (p=0.002, MAF=0.20) and rs11908352 on chromosome 20 (p=0.002, MAF=0.21). Rs11908352 is located near the gene encoding MMP-9. Serum levels of MMP-9 were significantly associated with the rs11908352 genotypes (p=0.007). Conclusions These data indicate that two loci that confer risk to other autoimmune diseases also affect the severity of joint destruction in RA. Rs11908352 may influence joint destruction via MMP-9 production.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2013-203375</identifier><identifier>PMID: 23696630</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Adult ; Aged ; Arthritis, Rheumatoid - blood ; Arthritis, Rheumatoid - diagnostic imaging ; Arthritis, Rheumatoid - genetics ; Autoimmune diseases ; Disease ; Disease Progression ; Female ; Foot Joints - diagnostic imaging ; Gender ; Genetic Predisposition to Disease ; Genomes ; Genotype ; Hand Joints - diagnostic imaging ; Humans ; Hypotheses ; Male ; Matrix Metalloproteinase 9 - blood ; Matrix Metalloproteinase 9 - genetics ; Middle Aged ; Patients ; Polymorphism, Single Nucleotide ; Quality control ; Radiography ; Rheumatism ; Rheumatology ; Severity of Illness Index ; Studies</subject><ispartof>Annals of the rheumatic diseases, 2014-06, Vol.73 (6), p.1163-1169</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Copyright: 2014 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b384t-58f1d03e8d93fcf39d981f3b94605567e48e5b2e59b53dd7253b10b935f1cd0c3</citedby><cites>FETCH-LOGICAL-b384t-58f1d03e8d93fcf39d981f3b94605567e48e5b2e59b53dd7253b10b935f1cd0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/73/6/1163.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/73/6/1163.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,315,782,786,3198,23578,27931,27932,77608,77639</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23696630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Rooy, D P C</creatorcontrib><creatorcontrib>Zhernakova, A</creatorcontrib><creatorcontrib>Tsonaka, R</creatorcontrib><creatorcontrib>Willemze, A</creatorcontrib><creatorcontrib>Kurreeman, B A S</creatorcontrib><creatorcontrib>Trynka, G</creatorcontrib><creatorcontrib>van Toorn, L</creatorcontrib><creatorcontrib>Toes, R E M</creatorcontrib><creatorcontrib>Huizinga, T W J</creatorcontrib><creatorcontrib>Houwing-Duistermaat, J J</creatorcontrib><creatorcontrib>Gregersen, P K</creatorcontrib><creatorcontrib>van der Helm-van Mil, A H M</creatorcontrib><title>A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Objectives The severity of joint destruction is highly variable between rheumatoid arthritis (RA) patients. The majority of its heritability is still unexplained. Several autoimmune diseases share genetic risk variants that may also influence disease progression. We aimed to identify genetic risk factors for the severity of joint damage in RA by studying genetic susceptibility loci of several autoimmune diseases. Methods In phase 1, 3143 sets of x-rays of 646 Dutch RA patients taken over 7 years (Sharp van der Heijde (SHS) scored) were studied. Genotyping was done by Immunochip. Associations of single-nucleotide polymorphisms (SNPs) with minor allele frequency (MAF) >0.01 and joint destruction were analysed. In phase 2, 686 North American RA patients with 926 SHS-scored x-rays over 15 years of follow-up were evaluated. In both phases multiple testing corrections were done for the number of uncorrelated SNPs; the thresholds for significance were p<1.1×10−6 and p<0.0036. Matrix metalloproteinase 9 (MMP-9) levels were measured with ELISA in baseline serum samples. Results In phase 1, 109 SNPs associated significantly with joint destruction (p<1.1×10−6). Of these, 76 were located in the HLA region; the 33 non-HLA variants were studied in phase 2. Here two variants were associated with the severity of joint destruction: rs451066 on chromosome 14 (p=0.002, MAF=0.20) and rs11908352 on chromosome 20 (p=0.002, MAF=0.21). Rs11908352 is located near the gene encoding MMP-9. Serum levels of MMP-9 were significantly associated with the rs11908352 genotypes (p=0.007). Conclusions These data indicate that two loci that confer risk to other autoimmune diseases also affect the severity of joint destruction in RA. Rs11908352 may influence joint destruction via MMP-9 production.</description><subject>Adult</subject><subject>Aged</subject><subject>Arthritis, Rheumatoid - blood</subject><subject>Arthritis, Rheumatoid - diagnostic imaging</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Autoimmune diseases</subject><subject>Disease</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Foot Joints - diagnostic imaging</subject><subject>Gender</subject><subject>Genetic Predisposition to Disease</subject><subject>Genomes</subject><subject>Genotype</subject><subject>Hand Joints - diagnostic imaging</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Male</subject><subject>Matrix Metalloproteinase 9 - blood</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Quality control</subject><subject>Radiography</subject><subject>Rheumatism</subject><subject>Rheumatology</subject><subject>Severity of Illness Index</subject><subject>Studies</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkUFv1DAQhS0EokvhL4AlLlwCdia242NVFYrUCg5wtpx4sutVYhfbacWNn46XXRDixGVGo_ne05MeIa84e8s5yHc2hLTDdXE-Ny3jUAeAEo_Ihneyr5dkj8mGMQZNp6U6I89y3teT9bx_Ss5akFpKYBvy44JuMWDxI723ydtQqA-07JAm3PoYaJzo7e3nRlOfqc05jt4WdPTBlx3NmNaFzniPc30GR-9S3CbM-STcR1_9nF3sFg-2vyLbEr2jNpVd8sXn5-TJZOeML077nHx9f_Xl8rq5-fTh4-XFTTNA35VG9BN3DLB3GqZxAu10zycYdCeZEFJh16MYWhR6EOCcagUMnA0axMRHx0Y4J2-OvjXjtxVzMYvPI86zDRjXbLhoObRCdH1FX_-D7uOaQk1nuFJKM9UpqJQ6UmOKOSeczF3yi03fDWfmUJL5qyRzKMkcS6rKlyf_dVjQ_dH9bqUC7REYlv1_u_4E1NyhxQ</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>de Rooy, D P C</creator><creator>Zhernakova, A</creator><creator>Tsonaka, R</creator><creator>Willemze, A</creator><creator>Kurreeman, B A S</creator><creator>Trynka, G</creator><creator>van Toorn, L</creator><creator>Toes, R E M</creator><creator>Huizinga, T W J</creator><creator>Houwing-Duistermaat, J J</creator><creator>Gregersen, P K</creator><creator>van der Helm-van Mil, A H M</creator><general>BMJ Publishing Group 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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20140601</creationdate><title>A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis</title><author>de Rooy, D P C ; Zhernakova, A ; Tsonaka, R ; Willemze, A ; Kurreeman, B A S ; Trynka, G ; van Toorn, L ; Toes, R E M ; Huizinga, T W J ; Houwing-Duistermaat, J J ; Gregersen, P K ; van der Helm-van Mil, A H M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b384t-58f1d03e8d93fcf39d981f3b94605567e48e5b2e59b53dd7253b10b935f1cd0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Arthritis, Rheumatoid - blood</topic><topic>Arthritis, Rheumatoid - diagnostic imaging</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Autoimmune diseases</topic><topic>Disease</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Foot Joints - diagnostic imaging</topic><topic>Gender</topic><topic>Genetic Predisposition to Disease</topic><topic>Genomes</topic><topic>Genotype</topic><topic>Hand Joints - diagnostic imaging</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Male</topic><topic>Matrix Metalloproteinase 9 - blood</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Middle Aged</topic><topic>Patients</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Quality control</topic><topic>Radiography</topic><topic>Rheumatism</topic><topic>Rheumatology</topic><topic>Severity of Illness Index</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Rooy, D P C</creatorcontrib><creatorcontrib>Zhernakova, A</creatorcontrib><creatorcontrib>Tsonaka, R</creatorcontrib><creatorcontrib>Willemze, A</creatorcontrib><creatorcontrib>Kurreeman, B A S</creatorcontrib><creatorcontrib>Trynka, G</creatorcontrib><creatorcontrib>van Toorn, L</creatorcontrib><creatorcontrib>Toes, R E M</creatorcontrib><creatorcontrib>Huizinga, T W J</creatorcontrib><creatorcontrib>Houwing-Duistermaat, J J</creatorcontrib><creatorcontrib>Gregersen, P K</creatorcontrib><creatorcontrib>van der Helm-van Mil, A H 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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Rooy, D P C</au><au>Zhernakova, A</au><au>Tsonaka, R</au><au>Willemze, A</au><au>Kurreeman, B A S</au><au>Trynka, G</au><au>van Toorn, L</au><au>Toes, R E M</au><au>Huizinga, T W J</au><au>Houwing-Duistermaat, J J</au><au>Gregersen, P K</au><au>van der Helm-van Mil, A H M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>73</volume><issue>6</issue><spage>1163</spage><epage>1169</epage><pages>1163-1169</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Objectives The severity of joint destruction is highly variable between rheumatoid arthritis (RA) patients. The majority of its heritability is still unexplained. Several autoimmune diseases share genetic risk variants that may also influence disease progression. We aimed to identify genetic risk factors for the severity of joint damage in RA by studying genetic susceptibility loci of several autoimmune diseases. Methods In phase 1, 3143 sets of x-rays of 646 Dutch RA patients taken over 7 years (Sharp van der Heijde (SHS) scored) were studied. Genotyping was done by Immunochip. Associations of single-nucleotide polymorphisms (SNPs) with minor allele frequency (MAF) >0.01 and joint destruction were analysed. In phase 2, 686 North American RA patients with 926 SHS-scored x-rays over 15 years of follow-up were evaluated. In both phases multiple testing corrections were done for the number of uncorrelated SNPs; the thresholds for significance were p<1.1×10−6 and p<0.0036. Matrix metalloproteinase 9 (MMP-9) levels were measured with ELISA in baseline serum samples. Results In phase 1, 109 SNPs associated significantly with joint destruction (p<1.1×10−6). Of these, 76 were located in the HLA region; the 33 non-HLA variants were studied in phase 2. Here two variants were associated with the severity of joint destruction: rs451066 on chromosome 14 (p=0.002, MAF=0.20) and rs11908352 on chromosome 20 (p=0.002, MAF=0.21). Rs11908352 is located near the gene encoding MMP-9. Serum levels of MMP-9 were significantly associated with the rs11908352 genotypes (p=0.007). Conclusions These data indicate that two loci that confer risk to other autoimmune diseases also affect the severity of joint destruction in RA. Rs11908352 may influence joint destruction via MMP-9 production.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>23696630</pmid><doi>10.1136/annrheumdis-2013-203375</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Aged Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - diagnostic imaging Arthritis, Rheumatoid - genetics Autoimmune diseases Disease Disease Progression Female Foot Joints - diagnostic imaging Gender Genetic Predisposition to Disease Genomes Genotype Hand Joints - diagnostic imaging Humans Hypotheses Male Matrix Metalloproteinase 9 - blood Matrix Metalloproteinase 9 - genetics Middle Aged Patients Polymorphism, Single Nucleotide Quality control Radiography Rheumatism Rheumatology Severity of Illness Index Studies |
| title | A genetic variant in the region of MMP-9 is associated with serum levels and progression of joint damage in rheumatoid arthritis |
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