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
Hauptverfasser: 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
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container_end_page 1169
container_issue 6
container_start_page 1163
container_title Annals of the rheumatic diseases
container_volume 73
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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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) &gt;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&lt;1.1×10−6 and p&lt;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&lt;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) &gt;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&lt;1.1×10−6 and p&lt;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&lt;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 &amp; 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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) &gt;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&lt;1.1×10−6 and p&lt;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&lt;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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