CTGF increases IL-6 expression in human synovial fibroblasts through integrin-dependent signaling pathway
Connective tissue growth factor (CTGF; also known as CCN2) is an inflammatory mediator, and shows elevated levels in regions of severe injury and inflammatory diseases. CTGF is abundantly expressed in osteoarthritis (OA). However, the relationship between CTGF and IL-6 in OA synovial fibroblasts (OA...
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| creator | Liu, Shan-Chi Hsu, Chin-Jung Chen, Hsien-Te Tsou, Hsi-Kai Chuang, Show-Mei Tang, Chih-Hsin |
| description | Connective tissue growth factor (CTGF; also known as CCN2) is an inflammatory mediator, and shows elevated levels in regions of severe injury and inflammatory diseases. CTGF is abundantly expressed in osteoarthritis (OA). However, the relationship between CTGF and IL-6 in OA synovial fibroblasts (OASFs) is mostly unknown.
OASFs showed significant expression of CTGF, and expression was higher than in normal SFs. OASFs stimulation with CTGF induced concentration-dependent increases in IL-6 expression. CTGF mediated IL-6 production was attenuated by αvβ5 integrin neutralized antibody and apoptosis signal-regulating kinase 1 (ASK1) shRNA. Pretreatment with p38 inhibitor (SB203580), JNK inhibitor (SP600125), AP-1 inhibitors (Curcumin and Tanshinone IIA), and NF-κB inhibitors (PDTC and TPCK) also inhibited the potentiating action of CTGF. CTGF-mediated increase of NF-κB and AP-1 luciferase activity was inhibited by SB203580 and SP600125 or ASK1 shRNA or p38 and JNK mutant.
Our results suggest that CTGF increased IL-6 production in OASFs via the αvβ5 integrin, ASK1, p38/JNK, and AP-1/NF-κB signaling pathways. |
| doi_str_mv | 10.1371/journal.pone.0051097 |
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OASFs showed significant expression of CTGF, and expression was higher than in normal SFs. OASFs stimulation with CTGF induced concentration-dependent increases in IL-6 expression. CTGF mediated IL-6 production was attenuated by αvβ5 integrin neutralized antibody and apoptosis signal-regulating kinase 1 (ASK1) shRNA. Pretreatment with p38 inhibitor (SB203580), JNK inhibitor (SP600125), AP-1 inhibitors (Curcumin and Tanshinone IIA), and NF-κB inhibitors (PDTC and TPCK) also inhibited the potentiating action of CTGF. CTGF-mediated increase of NF-κB and AP-1 luciferase activity was inhibited by SB203580 and SP600125 or ASK1 shRNA or p38 and JNK mutant.
Our results suggest that CTGF increased IL-6 production in OASFs via the αvβ5 integrin, ASK1, p38/JNK, and AP-1/NF-κB signaling pathways.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0051097</identifier><identifier>PMID: 23227240</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antibodies ; Apoptosis ; Arthritis ; Biocompatibility ; Biology ; Biomedical materials ; Bone surgery ; Cancer ; Community colleges ; Connective tissue growth factor ; Connective Tissue Growth Factor - pharmacology ; Connective tissues ; Curcumin ; Cytokines ; Fibroblasts ; Fibroblasts - drug effects ; Fibroblasts - enzymology ; Fibroblasts - metabolism ; Gene expression ; Growth factors ; Hospitals ; Humans ; Inflammation ; Inflammatory diseases ; Inhibitors ; Integrins ; Interleukin 6 ; Interleukin-6 - biosynthesis ; Interleukin-6 - metabolism ; JNK Mitogen-Activated Protein Kinases - metabolism ; JNK protein ; Kinases ; Luciferase ; MAP kinase ; MAP Kinase Kinase Kinase 5 - metabolism ; MAP Kinase Signaling System - drug effects ; Materials science ; Medicine ; Models, Biological ; Mutation ; NF-kappa B - metabolism ; NF-κB protein ; Orthopedics ; Osteoarthritis ; p38 Mitogen-Activated Protein Kinases - metabolism ; Polyclonal antibodies ; Receptors, Vitronectin - metabolism ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Synovial Membrane - pathology ; Transcription Factor AP-1 - metabolism ; Transcription factors ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2012-12, Vol.7 (12), p.e51097-e51097</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Liu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>2012 Liu et al 2012 Liu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c809t-c1fcaeaa8d24b3740aafd73abb0476b6b395e402c50c52cb878d18598dd1fd3d3</citedby><cites>FETCH-LOGICAL-c809t-c1fcaeaa8d24b3740aafd73abb0476b6b395e402c50c52cb878d18598dd1fd3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515445/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515445/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23227240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Tsilibary, Effie C.</contributor><creatorcontrib>Liu, Shan-Chi</creatorcontrib><creatorcontrib>Hsu, Chin-Jung</creatorcontrib><creatorcontrib>Chen, Hsien-Te</creatorcontrib><creatorcontrib>Tsou, Hsi-Kai</creatorcontrib><creatorcontrib>Chuang, Show-Mei</creatorcontrib><creatorcontrib>Tang, Chih-Hsin</creatorcontrib><title>CTGF increases IL-6 expression in human synovial fibroblasts through integrin-dependent signaling pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Connective tissue growth factor (CTGF; also known as CCN2) is an inflammatory mediator, and shows elevated levels in regions of severe injury and inflammatory diseases. CTGF is abundantly expressed in osteoarthritis (OA). However, the relationship between CTGF and IL-6 in OA synovial fibroblasts (OASFs) is mostly unknown.
OASFs showed significant expression of CTGF, and expression was higher than in normal SFs. OASFs stimulation with CTGF induced concentration-dependent increases in IL-6 expression. CTGF mediated IL-6 production was attenuated by αvβ5 integrin neutralized antibody and apoptosis signal-regulating kinase 1 (ASK1) shRNA. Pretreatment with p38 inhibitor (SB203580), JNK inhibitor (SP600125), AP-1 inhibitors (Curcumin and Tanshinone IIA), and NF-κB inhibitors (PDTC and TPCK) also inhibited the potentiating action of CTGF. CTGF-mediated increase of NF-κB and AP-1 luciferase activity was inhibited by SB203580 and SP600125 or ASK1 shRNA or p38 and JNK mutant.
Our results suggest that CTGF increased IL-6 production in OASFs via the αvβ5 integrin, ASK1, p38/JNK, and AP-1/NF-κB signaling pathways.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Arthritis</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>Biomedical materials</subject><subject>Bone surgery</subject><subject>Cancer</subject><subject>Community colleges</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - pharmacology</subject><subject>Connective tissues</subject><subject>Curcumin</subject><subject>Cytokines</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - enzymology</subject><subject>Fibroblasts - metabolism</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Inhibitors</subject><subject>Integrins</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Interleukin-6 - metabolism</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Luciferase</subject><subject>MAP kinase</subject><subject>MAP Kinase Kinase Kinase 5 - metabolism</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Materials science</subject><subject>Medicine</subject><subject>Models, Biological</subject><subject>Mutation</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Orthopedics</subject><subject>Osteoarthritis</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Polyclonal antibodies</subject><subject>Receptors, Vitronectin - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Synovial Membrane - pathology</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</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><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9-L1DAQx4so3nn6H4gWBNGHrvnRNO2LcBzeubBwoKevYZqkbZZusibtefvfm3V7x1buQfKQkPnMNzOTmSR5jdECU44_rd3oLfSLrbN6gRDDqOJPklNcUZIVBNGnR-eT5EUI6wjRsiieJyeEEsJJjk4Tc3FzdZkaK72GoEO6XGVFqu-2XodgnI2WtBs3YNOws-7WQJ82pvau7iEMIR0678a2i9SgW29spvRWW6XtkAbTxuiMbdMtDN1v2L1MnjXQB_1q2s-SH5dfbi6-Zqvrq-XF-SqTJaqGTOJGggYoFclrynME0ChOoa5Rzou6qGnFdI6IZEgyIuuSlwqXrCqVwo2iip4lbw-6294FMVUpCExJwRnOiyoSywOhHKzF1psN-J1wYMTfC-dbAX4wstcCtCoLpKEhROZQQY0Z45yiWLsG1bKJWp-n18Z6o5WMqXvoZ6JzizWdaN2toAyzPGdR4MMk4N2vUYdBbEyQuu_BajfGuAnlDPES7dF3_6CPZzdRLcQEjG1cfFfuRcV5zjmqYvB5pBaPUHEpvTEytlRj4v3M4ePMITKDvhtaGEMQy-_f_p-9_jln3x-xnYZ-6ILrxyF2X5iD-QGU3oXgdfNQZIzEfiLuqyH2EyGmiYhub44_6MHpfgToH6uNB6E</recordid><startdate>20121205</startdate><enddate>20121205</enddate><creator>Liu, Shan-Chi</creator><creator>Hsu, Chin-Jung</creator><creator>Chen, Hsien-Te</creator><creator>Tsou, Hsi-Kai</creator><creator>Chuang, Show-Mei</creator><creator>Tang, Chih-Hsin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121205</creationdate><title>CTGF increases IL-6 expression in human synovial fibroblasts through integrin-dependent signaling pathway</title><author>Liu, Shan-Chi ; Hsu, Chin-Jung ; Chen, Hsien-Te ; Tsou, Hsi-Kai ; Chuang, Show-Mei ; Tang, Chih-Hsin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c809t-c1fcaeaa8d24b3740aafd73abb0476b6b395e402c50c52cb878d18598dd1fd3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Arthritis</topic><topic>Biocompatibility</topic><topic>Biology</topic><topic>Biomedical materials</topic><topic>Bone surgery</topic><topic>Cancer</topic><topic>Community colleges</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - pharmacology</topic><topic>Connective tissues</topic><topic>Curcumin</topic><topic>Cytokines</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - enzymology</topic><topic>Fibroblasts - metabolism</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Inhibitors</topic><topic>Integrins</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Interleukin-6 - metabolism</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Luciferase</topic><topic>MAP kinase</topic><topic>MAP Kinase Kinase Kinase 5 - metabolism</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Materials science</topic><topic>Medicine</topic><topic>Models, Biological</topic><topic>Mutation</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Orthopedics</topic><topic>Osteoarthritis</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Polyclonal antibodies</topic><topic>Receptors, Vitronectin - metabolism</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Synovial Membrane - pathology</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shan-Chi</creatorcontrib><creatorcontrib>Hsu, Chin-Jung</creatorcontrib><creatorcontrib>Chen, Hsien-Te</creatorcontrib><creatorcontrib>Tsou, Hsi-Kai</creatorcontrib><creatorcontrib>Chuang, Show-Mei</creatorcontrib><creatorcontrib>Tang, Chih-Hsin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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 Edition)</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>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 Korea</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</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>Liu, Shan-Chi</au><au>Hsu, Chin-Jung</au><au>Chen, Hsien-Te</au><au>Tsou, Hsi-Kai</au><au>Chuang, Show-Mei</au><au>Tang, Chih-Hsin</au><au>Tsilibary, Effie C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CTGF increases IL-6 expression in human synovial fibroblasts through integrin-dependent signaling pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-12-05</date><risdate>2012</risdate><volume>7</volume><issue>12</issue><spage>e51097</spage><epage>e51097</epage><pages>e51097-e51097</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Connective tissue growth factor (CTGF; also known as CCN2) is an inflammatory mediator, and shows elevated levels in regions of severe injury and inflammatory diseases. CTGF is abundantly expressed in osteoarthritis (OA). However, the relationship between CTGF and IL-6 in OA synovial fibroblasts (OASFs) is mostly unknown.
OASFs showed significant expression of CTGF, and expression was higher than in normal SFs. OASFs stimulation with CTGF induced concentration-dependent increases in IL-6 expression. CTGF mediated IL-6 production was attenuated by αvβ5 integrin neutralized antibody and apoptosis signal-regulating kinase 1 (ASK1) shRNA. Pretreatment with p38 inhibitor (SB203580), JNK inhibitor (SP600125), AP-1 inhibitors (Curcumin and Tanshinone IIA), and NF-κB inhibitors (PDTC and TPCK) also inhibited the potentiating action of CTGF. CTGF-mediated increase of NF-κB and AP-1 luciferase activity was inhibited by SB203580 and SP600125 or ASK1 shRNA or p38 and JNK mutant.
Our results suggest that CTGF increased IL-6 production in OASFs via the αvβ5 integrin, ASK1, p38/JNK, and AP-1/NF-κB signaling pathways.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23227240</pmid><doi>10.1371/journal.pone.0051097</doi><tpages>e51097</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Antibodies Apoptosis Arthritis Biocompatibility Biology Biomedical materials Bone surgery Cancer Community colleges Connective tissue growth factor Connective Tissue Growth Factor - pharmacology Connective tissues Curcumin Cytokines Fibroblasts Fibroblasts - drug effects Fibroblasts - enzymology Fibroblasts - metabolism Gene expression Growth factors Hospitals Humans Inflammation Inflammatory diseases Inhibitors Integrins Interleukin 6 Interleukin-6 - biosynthesis Interleukin-6 - metabolism JNK Mitogen-Activated Protein Kinases - metabolism JNK protein Kinases Luciferase MAP kinase MAP Kinase Kinase Kinase 5 - metabolism MAP Kinase Signaling System - drug effects Materials science Medicine Models, Biological Mutation NF-kappa B - metabolism NF-κB protein Orthopedics Osteoarthritis p38 Mitogen-Activated Protein Kinases - metabolism Polyclonal antibodies Receptors, Vitronectin - metabolism Rodents Signal transduction Signal Transduction - drug effects Signaling Synovial Membrane - pathology Transcription Factor AP-1 - metabolism Transcription factors Tumor necrosis factor-TNF |
| title | CTGF increases IL-6 expression in human synovial fibroblasts through integrin-dependent signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T14%3A29%3A42IST&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=CTGF%20increases%20IL-6%20expression%20in%20human%20synovial%20fibroblasts%20through%20integrin-dependent%20signaling%20pathway&rft.jtitle=PloS%20one&rft.au=Liu,%20Shan-Chi&rft.date=2012-12-05&rft.volume=7&rft.issue=12&rft.spage=e51097&rft.epage=e51097&rft.pages=e51097-e51097&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0051097&rft_dat=%3Cgale_plos_%3EA477090244%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=1326751469&rft_id=info:pmid/23227240&rft_galeid=A477090244&rft_doaj_id=oai_doaj_org_article_aed860eaf22c4a9ab1557730240f0bcf&rfr_iscdi=true |