CCN1 induces oncostatin M production in osteoblasts via integrin-dependent signal pathways
Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1...
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| description | Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment. |
| doi_str_mv | 10.1371/journal.pone.0106632 |
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Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0106632</identifier><identifier>PMID: 25187949</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; Apoptosis ; Arthritis ; Biocompatibility ; Biology and Life Sciences ; Biotechnology ; Blotting, Western ; Bone surgery ; Cell adhesion & migration ; Cell culture ; Cell Line ; Chromatin Immunoprecipitation ; CYR61 protein ; Cysteine ; Cysteine-Rich Protein 61 - pharmacology ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Extracellular matrix ; Focal adhesion kinase ; Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors ; Focal Adhesion Protein-Tyrosine Kinases - metabolism ; Gene amplification ; Humans ; Inflammation ; Inflammatory response ; Integrins ; Integrins - metabolism ; Kinases ; Luciferase ; Medicine and Health Sciences ; Monoclonal antibodies ; Motility ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - metabolism ; NF-κB protein ; Oncostatin M ; Oncostatin M - genetics ; Oncostatin M - metabolism ; Osteoarthritis ; Osteoblasts ; Osteoblasts - drug effects ; Osteoblasts - metabolism ; Pathogenesis ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Polyclonal antibodies ; Proteins ; Real-Time Polymerase Chain Reaction ; Rheumatoid arthritis ; Science ; Signal transduction ; Signal Transduction - drug effects ; Src protein ; Studies</subject><ispartof>PloS one, 2014-09, Vol.9 (9), p.e106632-e106632</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Chen 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>2014 Chen et al 2014 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-5800da1bd14b3b0769b374932d3d9b67776e7a04e6ef000db93ecc0eaa56ec223</citedby><cites>FETCH-LOGICAL-c758t-5800da1bd14b3b0769b374932d3d9b67776e7a04e6ef000db93ecc0eaa56ec223</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/PMC4154729/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4154729/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25187949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Cheng-Yu</creatorcontrib><creatorcontrib>Su, Chen-Ming</creatorcontrib><creatorcontrib>Huang, Yuan-Li</creatorcontrib><creatorcontrib>Tsai, Chun-Hao</creatorcontrib><creatorcontrib>Fuh, Lih-Jyh</creatorcontrib><creatorcontrib>Tang, Chih-Hsin</creatorcontrib><title>CCN1 induces oncostatin M production in osteoblasts via integrin-dependent signal pathways</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Apoptosis</subject><subject>Arthritis</subject><subject>Biocompatibility</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>Bone surgery</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Chromatin Immunoprecipitation</subject><subject>CYR61 protein</subject><subject>Cysteine</subject><subject>Cysteine-Rich Protein 61 - pharmacology</subject><subject>Cytokines</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Extracellular matrix</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - metabolism</subject><subject>Gene amplification</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Integrins</subject><subject>Integrins - metabolism</subject><subject>Kinases</subject><subject>Luciferase</subject><subject>Medicine and Health Sciences</subject><subject>Monoclonal antibodies</subject><subject>Motility</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oncostatin M</subject><subject>Oncostatin M - genetics</subject><subject>Oncostatin M - metabolism</subject><subject>Osteoarthritis</subject><subject>Osteoblasts</subject><subject>Osteoblasts - drug effects</subject><subject>Osteoblasts - metabolism</subject><subject>Pathogenesis</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Rheumatoid arthritis</subject><subject>Science</subject><subject>Signal transduction</subject><subject>Signal Transduction - 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pharmacology</topic><topic>Cytokines</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Extracellular matrix</topic><topic>Focal adhesion kinase</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - metabolism</topic><topic>Gene amplification</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Integrins</topic><topic>Integrins - metabolism</topic><topic>Kinases</topic><topic>Luciferase</topic><topic>Medicine and Health Sciences</topic><topic>Monoclonal antibodies</topic><topic>Motility</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oncostatin M</topic><topic>Oncostatin M - genetics</topic><topic>Oncostatin M - metabolism</topic><topic>Osteoarthritis</topic><topic>Osteoblasts</topic><topic>Osteoblasts - drug effects</topic><topic>Osteoblasts - metabolism</topic><topic>Pathogenesis</topic><topic>Phosphatidylinositol 3-Kinases - 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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>Chen, Cheng-Yu</au><au>Su, Chen-Ming</au><au>Huang, Yuan-Li</au><au>Tsai, Chun-Hao</au><au>Fuh, Lih-Jyh</au><au>Tang, Chih-Hsin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCN1 induces oncostatin M production in osteoblasts via integrin-dependent signal pathways</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-09-04</date><risdate>2014</risdate><volume>9</volume><issue>9</issue><spage>e106632</spage><epage>e106632</epage><pages>e106632-e106632</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25187949</pmid><doi>10.1371/journal.pone.0106632</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | 1-Phosphatidylinositol 3-kinase Apoptosis Arthritis Biocompatibility Biology and Life Sciences Biotechnology Blotting, Western Bone surgery Cell adhesion & migration Cell culture Cell Line Chromatin Immunoprecipitation CYR61 protein Cysteine Cysteine-Rich Protein 61 - pharmacology Cytokines Enzyme-Linked Immunosorbent Assay Extracellular matrix Focal adhesion kinase Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors Focal Adhesion Protein-Tyrosine Kinases - metabolism Gene amplification Humans Inflammation Inflammatory response Integrins Integrins - metabolism Kinases Luciferase Medicine and Health Sciences Monoclonal antibodies Motility NF-kappa B - antagonists & inhibitors NF-kappa B - metabolism NF-κB protein Oncostatin M Oncostatin M - genetics Oncostatin M - metabolism Osteoarthritis Osteoblasts Osteoblasts - drug effects Osteoblasts - metabolism Pathogenesis Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Polyclonal antibodies Proteins Real-Time Polymerase Chain Reaction Rheumatoid arthritis Science Signal transduction Signal Transduction - drug effects Src protein Studies |
| title | CCN1 induces oncostatin M production in osteoblasts via integrin-dependent signal pathways |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T06%3A13%3A44IST&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=CCN1%20induces%20oncostatin%20M%20production%20in%20osteoblasts%20via%20integrin-dependent%20signal%20pathways&rft.jtitle=PloS%20one&rft.au=Chen,%20Cheng-Yu&rft.date=2014-09-04&rft.volume=9&rft.issue=9&rft.spage=e106632&rft.epage=e106632&rft.pages=e106632-e106632&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0106632&rft_dat=%3Cgale_plos_%3EA416975678%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=1560107141&rft_id=info:pmid/25187949&rft_galeid=A416975678&rft_doaj_id=oai_doaj_org_article_66f4f11e815748bba2026e508d325230&rfr_iscdi=true |