Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis
The endothelial glycocalyx (EG) is essential for proper function of the endothelium and for vascular integrity, but its role in premature atherogenesis in rheumatoid arthritis (RA) has not been studied yet. EG impairment can play a role in pathogenesis of vascular disease, and one of its characteris...
Gespeichert in:
| Veröffentlicht in: | PloS one 2021-07, Vol.16 (7), p.e0253247-e0253247 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0253247 |
|---|---|
| container_issue | 7 |
| container_start_page | e0253247 |
| container_title | PloS one |
| container_volume | 16 |
| creator | Deyab, Gia Reine, Trine Marita Vuong, Tram Thu Jenssen, Trond Hjeltnes, Gunnbjørg Agewall, Stefan Mikkelsen, Knut Førre, Øystein Fagerland, Morten Wang Kolset, Svein Olav Hollan, Ivana |
| description | The endothelial glycocalyx (EG) is essential for proper function of the endothelium and for vascular integrity, but its role in premature atherogenesis in rheumatoid arthritis (RA) has not been studied yet. EG impairment can play a role in pathogenesis of vascular disease, and one of its characteristics is shedding of syndecan-1 from endothelial cells. Syndecan-1 shedding is mediated by matrix metalloproteinase-9 (MMP-9) and counteracted by tissue inhibitor of metalloproteinases (TIMP)-1. Cardiovascular disease risk in RA is reversible by disease modifying antirheumatic drugs (DMARDs), but the exact modes of action are still unclear. Therefore, we examined effects of DMARDs on syndecan-1, MMP-9 and TIMP-1 in RA patients, and searched for associations between these parameters and inflammatory activity. From the observational PSARA study, we examined 39 patients starting with methotrexate (MTX) monotherapy (in MTX naïve patients, n = 19) or tumor necrosis factor inhibitors (TNFi) in combination with MTX (in MTX non-responders, n = 20) due to active RA. Serum syndecan-1, MMP-9 and TIMP-1 were measured at baseline and after six weeks of treatment. Serum syndecan-1 (p = 0.008) and TIMP-1 (p |
| doi_str_mv | 10.1371/journal.pone.0253247 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_gale_infotracmisc_A667980282</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A667980282</galeid><doaj_id>oai_doaj_org_article_4f73757932ab476da0063beea41a4747</doaj_id><sourcerecordid>A667980282</sourcerecordid><originalsourceid>FETCH-LOGICAL-c781t-d86e324fd3fa02deec7f8e5a992ab8aa77a91e20404ef7e0f593ac799dd852563</originalsourceid><addsrcrecordid>eNqNk0tv1DAUhSMEoqXwD5CIhIRgMYNfieMN0qjiUalSpRbYsLDuxDczLkk8tR1K_z0eJkMbVCSUReyb75zYx75Z9pySOeWSvr10g--hnW9cj3PCCs6EfJAdUsXZrGSEP7wzPsiehHBJSMGrsnycHXDBBGOiPMy-Lfpo_RqHDqKt8-gRYod9zG3IIQRXW4ho8msb17lHM9RpEtAPXX5x0xusoZ_R3Pb5-c7CWZMvfFx7G214mj1qoA34bHwfZV8-vP98_Gl2evbx5HhxOqtlRePMVCWmxTeGN0CYQaxlU2EBSjFYVgBSgqLIiCACG4mkKRSHWiplTFWwouRH2Yud76Z1QY-5BM0KoRQvS6EScbIjjINLvfG2A3-jHVj9u-D8SoNP-29Ri0ZyWciUHCyFLA0QUvIlIggKQgqZvGY7r3CNm2E5cRtL39MIdXIhhCde_ZPfeGduRXshFZJKJkmVtO_GnQ3LDk2dDsZDO7WYfOntWq_cD10lOS3kbTS1tyHaXvfOg6ZpXVIzQUqaiNfjL7y7GjBE3dlQY9tCj27Ypliky6WIKhL68i_0_qxHagUpTts3Lq2s3prqRVlKVRFWsUTN76HSY7CzdbrSjU31ieDNRJCYiD_jCoYQ9MnF-f-zZ1-n7Ks77Bqhjevg2iFa14cpKPZRuhA8Nn-OgRK97ch9GnrbkXrsSP4LdqYnKg</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2549936649</pqid></control><display><type>article</type><title>Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis</title><source>PLoS</source><source>NORA - Norwegian Open Research Archives</source><source>DOAJ Directory of Open Access Journals</source><source>PubMed Central</source><source>SWEPUB Freely available online</source><source>Free Full-Text Journals in Chemistry</source><source>EZB Electronic Journals Library</source><creator>Deyab, Gia ; Reine, Trine Marita ; Vuong, Tram Thu ; Jenssen, Trond ; Hjeltnes, Gunnbjørg ; Agewall, Stefan ; Mikkelsen, Knut ; Førre, Øystein ; Fagerland, Morten Wang ; Kolset, Svein Olav ; Hollan, Ivana</creator><contributor>Kuwana, Masataka</contributor><creatorcontrib>Deyab, Gia ; Reine, Trine Marita ; Vuong, Tram Thu ; Jenssen, Trond ; Hjeltnes, Gunnbjørg ; Agewall, Stefan ; Mikkelsen, Knut ; Førre, Øystein ; Fagerland, Morten Wang ; Kolset, Svein Olav ; Hollan, Ivana ; Kuwana, Masataka</creatorcontrib><description>The endothelial glycocalyx (EG) is essential for proper function of the endothelium and for vascular integrity, but its role in premature atherogenesis in rheumatoid arthritis (RA) has not been studied yet. EG impairment can play a role in pathogenesis of vascular disease, and one of its characteristics is shedding of syndecan-1 from endothelial cells. Syndecan-1 shedding is mediated by matrix metalloproteinase-9 (MMP-9) and counteracted by tissue inhibitor of metalloproteinases (TIMP)-1. Cardiovascular disease risk in RA is reversible by disease modifying antirheumatic drugs (DMARDs), but the exact modes of action are still unclear. Therefore, we examined effects of DMARDs on syndecan-1, MMP-9 and TIMP-1 in RA patients, and searched for associations between these parameters and inflammatory activity. From the observational PSARA study, we examined 39 patients starting with methotrexate (MTX) monotherapy (in MTX naïve patients, n = 19) or tumor necrosis factor inhibitors (TNFi) in combination with MTX (in MTX non-responders, n = 20) due to active RA. Serum syndecan-1, MMP-9 and TIMP-1 were measured at baseline and after six weeks of treatment. Serum syndecan-1 (p = 0.008) and TIMP-1 (p<0.001) levels decreased after six weeks of anti-rheumatic treatment. Levels of MMP-9 also decreased, but the difference was not statistically significant. The improvement in syndecan-1 levels were independent of changes in inflammatory activity. There was no significant difference in changes in syndecan-1 levels from baseline to 6 weeks between the MTX and TNFi groups, however the change was significant within the MTX group. Six weeks of antirheumatic treatment was associated with reduction in serum levels of syndecan-1, which might reflect reduced syndecan-1 shedding from EG. Thus, it is possible that EG-preserving properties of DMARDs might contribute to their cardioprotective effects. These effects may be at least partly independent of their anti-inflammatory actions. Our findings do not support the notion that syndecan-1 shedding in RA is mediated mainly by increased MMP-9 or decreased TIMP-9 serum concentration.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0253247</identifier><identifier>PMID: 34242246</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Antirheumatic agents ; Arthritis ; Atherogenesis ; Atherosclerosis ; Biology and Life Sciences ; Cardiovascular diseases ; Chemokines ; Chronic illnesses ; Disease ; Dosage and administration ; Drug therapy ; Endothelial cells ; Endothelium ; Gelatinase B ; Health aspects ; Health risks ; Health sciences ; Hospitals ; Inflammation ; Laboratories ; Matrix metalloproteinase ; Matrix metalloproteinases ; Measurement ; Medicin och hälsovetenskap ; Medicine ; Medicine and Health Sciences ; Membrane proteins ; Metabolism ; Metalloproteinase ; Methotrexate ; Mortality ; Nephrology ; Pathogenesis ; Patients ; Physical Sciences ; Physiological aspects ; R&D ; Research & development ; Research and Analysis Methods ; Rheumatoid arthritis ; Rheumatology ; Serum levels ; Shedding ; Statistical analysis ; Syndecan ; Tissue inhibitor of metalloproteinase 1 ; TNF inhibitors ; Tumor necrosis factor-TNF ; Vascular diseases</subject><ispartof>PloS one, 2021-07, Vol.16 (7), p.e0253247-e0253247</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Deyab et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>info:eu-repo/semantics/openAccess</rights><rights>2021 Deyab et al 2021 Deyab et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c781t-d86e324fd3fa02deec7f8e5a992ab8aa77a91e20404ef7e0f593ac799dd852563</citedby><cites>FETCH-LOGICAL-c781t-d86e324fd3fa02deec7f8e5a992ab8aa77a91e20404ef7e0f593ac799dd852563</cites><orcidid>0000-0002-6143-1600</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8270157/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8270157/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,553,728,781,785,865,886,2103,2929,23868,26569,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:147172708$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Kuwana, Masataka</contributor><creatorcontrib>Deyab, Gia</creatorcontrib><creatorcontrib>Reine, Trine Marita</creatorcontrib><creatorcontrib>Vuong, Tram Thu</creatorcontrib><creatorcontrib>Jenssen, Trond</creatorcontrib><creatorcontrib>Hjeltnes, Gunnbjørg</creatorcontrib><creatorcontrib>Agewall, Stefan</creatorcontrib><creatorcontrib>Mikkelsen, Knut</creatorcontrib><creatorcontrib>Førre, Øystein</creatorcontrib><creatorcontrib>Fagerland, Morten Wang</creatorcontrib><creatorcontrib>Kolset, Svein Olav</creatorcontrib><creatorcontrib>Hollan, Ivana</creatorcontrib><title>Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis</title><title>PloS one</title><description>The endothelial glycocalyx (EG) is essential for proper function of the endothelium and for vascular integrity, but its role in premature atherogenesis in rheumatoid arthritis (RA) has not been studied yet. EG impairment can play a role in pathogenesis of vascular disease, and one of its characteristics is shedding of syndecan-1 from endothelial cells. Syndecan-1 shedding is mediated by matrix metalloproteinase-9 (MMP-9) and counteracted by tissue inhibitor of metalloproteinases (TIMP)-1. Cardiovascular disease risk in RA is reversible by disease modifying antirheumatic drugs (DMARDs), but the exact modes of action are still unclear. Therefore, we examined effects of DMARDs on syndecan-1, MMP-9 and TIMP-1 in RA patients, and searched for associations between these parameters and inflammatory activity. From the observational PSARA study, we examined 39 patients starting with methotrexate (MTX) monotherapy (in MTX naïve patients, n = 19) or tumor necrosis factor inhibitors (TNFi) in combination with MTX (in MTX non-responders, n = 20) due to active RA. Serum syndecan-1, MMP-9 and TIMP-1 were measured at baseline and after six weeks of treatment. Serum syndecan-1 (p = 0.008) and TIMP-1 (p<0.001) levels decreased after six weeks of anti-rheumatic treatment. Levels of MMP-9 also decreased, but the difference was not statistically significant. The improvement in syndecan-1 levels were independent of changes in inflammatory activity. There was no significant difference in changes in syndecan-1 levels from baseline to 6 weeks between the MTX and TNFi groups, however the change was significant within the MTX group. Six weeks of antirheumatic treatment was associated with reduction in serum levels of syndecan-1, which might reflect reduced syndecan-1 shedding from EG. Thus, it is possible that EG-preserving properties of DMARDs might contribute to their cardioprotective effects. These effects may be at least partly independent of their anti-inflammatory actions. Our findings do not support the notion that syndecan-1 shedding in RA is mediated mainly by increased MMP-9 or decreased TIMP-9 serum concentration.</description><subject>Antirheumatic agents</subject><subject>Arthritis</subject><subject>Atherogenesis</subject><subject>Atherosclerosis</subject><subject>Biology and Life Sciences</subject><subject>Cardiovascular diseases</subject><subject>Chemokines</subject><subject>Chronic illnesses</subject><subject>Disease</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Gelatinase B</subject><subject>Health aspects</subject><subject>Health risks</subject><subject>Health sciences</subject><subject>Hospitals</subject><subject>Inflammation</subject><subject>Laboratories</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Measurement</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Membrane proteins</subject><subject>Metabolism</subject><subject>Metalloproteinase</subject><subject>Methotrexate</subject><subject>Mortality</subject><subject>Nephrology</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Physical Sciences</subject><subject>Physiological aspects</subject><subject>R&D</subject><subject>Research & development</subject><subject>Research and Analysis Methods</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>Serum levels</subject><subject>Shedding</subject><subject>Statistical analysis</subject><subject>Syndecan</subject><subject>Tissue inhibitor of metalloproteinase 1</subject><subject>TNF inhibitors</subject><subject>Tumor necrosis factor-TNF</subject><subject>Vascular diseases</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>3HK</sourceid><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNqNk0tv1DAUhSMEoqXwD5CIhIRgMYNfieMN0qjiUalSpRbYsLDuxDczLkk8tR1K_z0eJkMbVCSUReyb75zYx75Z9pySOeWSvr10g--hnW9cj3PCCs6EfJAdUsXZrGSEP7wzPsiehHBJSMGrsnycHXDBBGOiPMy-Lfpo_RqHDqKt8-gRYod9zG3IIQRXW4ho8msb17lHM9RpEtAPXX5x0xusoZ_R3Pb5-c7CWZMvfFx7G214mj1qoA34bHwfZV8-vP98_Gl2evbx5HhxOqtlRePMVCWmxTeGN0CYQaxlU2EBSjFYVgBSgqLIiCACG4mkKRSHWiplTFWwouRH2Yud76Z1QY-5BM0KoRQvS6EScbIjjINLvfG2A3-jHVj9u-D8SoNP-29Ri0ZyWciUHCyFLA0QUvIlIggKQgqZvGY7r3CNm2E5cRtL39MIdXIhhCde_ZPfeGduRXshFZJKJkmVtO_GnQ3LDk2dDsZDO7WYfOntWq_cD10lOS3kbTS1tyHaXvfOg6ZpXVIzQUqaiNfjL7y7GjBE3dlQY9tCj27Ypliky6WIKhL68i_0_qxHagUpTts3Lq2s3prqRVlKVRFWsUTN76HSY7CzdbrSjU31ieDNRJCYiD_jCoYQ9MnF-f-zZ1-n7Ks77Bqhjevg2iFa14cpKPZRuhA8Nn-OgRK97ch9GnrbkXrsSP4LdqYnKg</recordid><startdate>20210709</startdate><enddate>20210709</enddate><creator>Deyab, Gia</creator><creator>Reine, Trine Marita</creator><creator>Vuong, Tram Thu</creator><creator>Jenssen, Trond</creator><creator>Hjeltnes, Gunnbjørg</creator><creator>Agewall, Stefan</creator><creator>Mikkelsen, Knut</creator><creator>Førre, Øystein</creator><creator>Fagerland, Morten Wang</creator><creator>Kolset, Svein Olav</creator><creator>Hollan, Ivana</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-6143-1600</orcidid></search><sort><creationdate>20210709</creationdate><title>Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis</title><author>Deyab, Gia ; Reine, Trine Marita ; Vuong, Tram Thu ; Jenssen, Trond ; Hjeltnes, Gunnbjørg ; Agewall, Stefan ; Mikkelsen, Knut ; Førre, Øystein ; Fagerland, Morten Wang ; Kolset, Svein Olav ; Hollan, Ivana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c781t-d86e324fd3fa02deec7f8e5a992ab8aa77a91e20404ef7e0f593ac799dd852563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antirheumatic agents</topic><topic>Arthritis</topic><topic>Atherogenesis</topic><topic>Atherosclerosis</topic><topic>Biology and Life Sciences</topic><topic>Cardiovascular diseases</topic><topic>Chemokines</topic><topic>Chronic illnesses</topic><topic>Disease</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Gelatinase B</topic><topic>Health aspects</topic><topic>Health risks</topic><topic>Health sciences</topic><topic>Hospitals</topic><topic>Inflammation</topic><topic>Laboratories</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Measurement</topic><topic>Medicin och hälsovetenskap</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Membrane proteins</topic><topic>Metabolism</topic><topic>Metalloproteinase</topic><topic>Methotrexate</topic><topic>Mortality</topic><topic>Nephrology</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Physical Sciences</topic><topic>Physiological aspects</topic><topic>R&D</topic><topic>Research & development</topic><topic>Research and Analysis Methods</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>Serum levels</topic><topic>Shedding</topic><topic>Statistical analysis</topic><topic>Syndecan</topic><topic>Tissue inhibitor of metalloproteinase 1</topic><topic>TNF inhibitors</topic><topic>Tumor necrosis factor-TNF</topic><topic>Vascular diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deyab, Gia</creatorcontrib><creatorcontrib>Reine, Trine Marita</creatorcontrib><creatorcontrib>Vuong, Tram Thu</creatorcontrib><creatorcontrib>Jenssen, Trond</creatorcontrib><creatorcontrib>Hjeltnes, Gunnbjørg</creatorcontrib><creatorcontrib>Agewall, Stefan</creatorcontrib><creatorcontrib>Mikkelsen, Knut</creatorcontrib><creatorcontrib>Førre, Øystein</creatorcontrib><creatorcontrib>Fagerland, Morten Wang</creatorcontrib><creatorcontrib>Kolset, Svein Olav</creatorcontrib><creatorcontrib>Hollan, Ivana</creatorcontrib><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Science (Gale in Context)</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>https://resources.nclive.org/materials</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials science collection</collection><collection>Publicly Available Content 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>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deyab, Gia</au><au>Reine, Trine Marita</au><au>Vuong, Tram Thu</au><au>Jenssen, Trond</au><au>Hjeltnes, Gunnbjørg</au><au>Agewall, Stefan</au><au>Mikkelsen, Knut</au><au>Førre, Øystein</au><au>Fagerland, Morten Wang</au><au>Kolset, Svein Olav</au><au>Hollan, Ivana</au><au>Kuwana, Masataka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis</atitle><jtitle>PloS one</jtitle><date>2021-07-09</date><risdate>2021</risdate><volume>16</volume><issue>7</issue><spage>e0253247</spage><epage>e0253247</epage><pages>e0253247-e0253247</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The endothelial glycocalyx (EG) is essential for proper function of the endothelium and for vascular integrity, but its role in premature atherogenesis in rheumatoid arthritis (RA) has not been studied yet. EG impairment can play a role in pathogenesis of vascular disease, and one of its characteristics is shedding of syndecan-1 from endothelial cells. Syndecan-1 shedding is mediated by matrix metalloproteinase-9 (MMP-9) and counteracted by tissue inhibitor of metalloproteinases (TIMP)-1. Cardiovascular disease risk in RA is reversible by disease modifying antirheumatic drugs (DMARDs), but the exact modes of action are still unclear. Therefore, we examined effects of DMARDs on syndecan-1, MMP-9 and TIMP-1 in RA patients, and searched for associations between these parameters and inflammatory activity. From the observational PSARA study, we examined 39 patients starting with methotrexate (MTX) monotherapy (in MTX naïve patients, n = 19) or tumor necrosis factor inhibitors (TNFi) in combination with MTX (in MTX non-responders, n = 20) due to active RA. Serum syndecan-1, MMP-9 and TIMP-1 were measured at baseline and after six weeks of treatment. Serum syndecan-1 (p = 0.008) and TIMP-1 (p<0.001) levels decreased after six weeks of anti-rheumatic treatment. Levels of MMP-9 also decreased, but the difference was not statistically significant. The improvement in syndecan-1 levels were independent of changes in inflammatory activity. There was no significant difference in changes in syndecan-1 levels from baseline to 6 weeks between the MTX and TNFi groups, however the change was significant within the MTX group. Six weeks of antirheumatic treatment was associated with reduction in serum levels of syndecan-1, which might reflect reduced syndecan-1 shedding from EG. Thus, it is possible that EG-preserving properties of DMARDs might contribute to their cardioprotective effects. These effects may be at least partly independent of their anti-inflammatory actions. Our findings do not support the notion that syndecan-1 shedding in RA is mediated mainly by increased MMP-9 or decreased TIMP-9 serum concentration.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>34242246</pmid><doi>10.1371/journal.pone.0253247</doi><tpages>e0253247</tpages><orcidid>https://orcid.org/0000-0002-6143-1600</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2021-07, Vol.16 (7), p.e0253247-e0253247 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_gale_infotracmisc_A667980282 |
| source | PLoS; NORA - Norwegian Open Research Archives; DOAJ Directory of Open Access Journals; PubMed Central; SWEPUB Freely available online; Free Full-Text Journals in Chemistry; EZB Electronic Journals Library |
| subjects | Antirheumatic agents Arthritis Atherogenesis Atherosclerosis Biology and Life Sciences Cardiovascular diseases Chemokines Chronic illnesses Disease Dosage and administration Drug therapy Endothelial cells Endothelium Gelatinase B Health aspects Health risks Health sciences Hospitals Inflammation Laboratories Matrix metalloproteinase Matrix metalloproteinases Measurement Medicin och hälsovetenskap Medicine Medicine and Health Sciences Membrane proteins Metabolism Metalloproteinase Methotrexate Mortality Nephrology Pathogenesis Patients Physical Sciences Physiological aspects R&D Research & development Research and Analysis Methods Rheumatoid arthritis Rheumatology Serum levels Shedding Statistical analysis Syndecan Tissue inhibitor of metalloproteinase 1 TNF inhibitors Tumor necrosis factor-TNF Vascular diseases |
| title | Antirheumatic treatment is associated with reduced serum Syndecan-1 in Rheumatoid Arthritis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T21%3A54%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antirheumatic%20treatment%20is%20associated%20with%20reduced%20serum%20Syndecan-1%20in%20Rheumatoid%20Arthritis&rft.jtitle=PloS%20one&rft.au=Deyab,%20Gia&rft.date=2021-07-09&rft.volume=16&rft.issue=7&rft.spage=e0253247&rft.epage=e0253247&rft.pages=e0253247-e0253247&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0253247&rft_dat=%3Cgale_plos_%3EA667980282%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2549936649&rft_id=info:pmid/34242246&rft_galeid=A667980282&rft_doaj_id=oai_doaj_org_article_4f73757932ab476da0063beea41a4747&rfr_iscdi=true |