{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T15:53:11Z","timestamp":1777477991625,"version":"3.51.4"},"reference-count":32,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2016,7,7]],"date-time":"2016-07-07T00:00:00Z","timestamp":1467849600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["CARTILAGE"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>RNA-binding protein with multiple splicing (RBPMS) has been shown to physically interact with Smads and enhance transforming growth factor-\u03b2 (TGF-\u03b2)\u2013mediated Smad2\/3 transcriptional activity in mammalian cells. Objective of this study was to examine whether expression of RBPMS is regulated by interleukin-1\u03b2 (IL)-1\u03b2 and TGF-\u03b2 superfamily growth factors and whether expression of RBPMS is altered during aging and experimental osteoarthritis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Expression of RBPMS protein was investigated in chondrocyte cell lines of murine (H4) and human (G6) origin using Western blot analysis. Regulation of RBPMS expression in H4 chondrocytes at mRNA level was done by reverse transcriptase\u2013quantitative polymerase chain reaction. Furthermore, characterization of Smad signaling pathways regulating RBPMS expression was performed by blocking studies using small molecule inhibitors or by transfection studies with adenoviral vector constructs (constitutive-active ALK1 and constitutive-active ALK5). Expression of RBPMS in cartilage of different age groups of C57BL\/6N mice (6 months and 20 months) and in a surgically induced osteoarthritis (OA) mouse model was analyzed using immunohistochemistry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>RBPMS was shown to be expressed in chondrocytes and cartilage of murine, human, and bovine origin. TGF-\u03b2 inhibited RBPMS expression while BMP2 and IL-1\u03b2 increased its expression. TGF-\u03b2-induced inhibition was blocked by ALK5 inhibitor. Overexpression of ca-ALK1 stimulated RBPMS expression. Moreover, RBPMS expression was found to be reduced with ageing and in OA pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Expression of RBPMS in chondrocytes is regulated by TGF-\u03b2 superfamily members and IL-1\u03b2, indicating a counter-regulatory mechanism. Expression of RBPMS, in cartilage and its reduction during ageing and OA might suggest its potential role in the maintenance of normal articular cartilage.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1947603515623991","type":"journal-article","created":{"date-parts":[[2016,2,24]],"date-time":"2016-02-24T22:18:42Z","timestamp":1456352322000},"page":"333-345","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":16,"title":["Expression of TGF-\u03b2 Signaling Regulator RBPMS (RNA-Binding Protein With Multiple Splicing) Is Regulated by IL-1\u03b2 and TGF-\u03b2 Superfamily Members, and Decreased in Aged and Osteoarthritic Cartilage"],"prefix":"10.1177","volume":"7","author":[{"given":"S.","family":"Shanmugaapriya","sequence":"first","affiliation":[{"name":"Department of Biomedical Science, Bharathidasan University, Tiruchirappalli, Tamil Nadu, India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"van Caam","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"de Kroon","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elly L.","family":"Vitters","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B","family":"Walgreen","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"van Beuningen","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. Blaney","family":"Davidson","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter M.","family":"van der Kraan","sequence":"additional","affiliation":[{"name":"Experimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2016,7,7]]},"reference":[{"key":"bibr1-1947603515623991","doi-asserted-by":"publisher","DOI":"10.1097\/00003086-200110001-00004"},{"key":"bibr2-1947603515623991","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-002-8400-3"},{"key":"bibr3-1947603515623991","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.153.1.35"},{"key":"bibr4-1947603515623991","doi-asserted-by":"crossref","unstructured":"Takahashi N1, Rieneck K, van der Kraan PM, van Beuningen HM, Vitters EL, Bendtzen K, Elucidation of IL-1\/TGF-\u03b2 interactions in mouse chondrocyte cell line by genome-wide gene expression. Osteoarthritis Cartilage. 2005;13(5):426-38.","DOI":"10.1016\/j.joca.2004.12.010"},{"key":"bibr5-1947603515623991","doi-asserted-by":"crossref","unstructured":"Goumans MJ, Valdimarsdottir G, Itoh S, Lebrin F, Larsson J, Mummery C, Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral TGF\u03b2\/ALK5 signaling. 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