{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T07:01:38Z","timestamp":1791356498947,"version":"4.3.1"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2002,7,1]],"date-time":"2002-07-01T00:00:00Z","timestamp":1025481600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Osteoarthritis has as main characteristics the degradation of articular cartilage and the formation of new bone at the joint edges, so-called osteophytes. In this study enhanced expression of TGF-\u03b21 and -\u03b23 was detected in developing osteophytes and articular cartilage during murine experimental osteoarthritis. To determine the role of endogenous TGF-\u03b2 on osteophyte formation and articular cartilage, TGF-\u03b2 activity was blocked via a scavenging soluble TGF-\u03b2-RII. Our results clearly show that inhibition of endogenous TGF-\u03b2 nearly completely prevented osteophyte formation. In contrast, treatment with recombinant soluble TGF-\u03b2-RII markedly enhanced articular cartilage proteoglycan loss and reduced the thickness of articular cartilage. In conclusion, we show for the first time that endogenous TGF-\u03b2 is a crucial factor in the process of osteophyte formation and has an important function in protection against cartilage loss.<\/jats:p>","DOI":"10.4049\/jimmunol.169.1.507","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:33:01Z","timestamp":1398025981000},"page":"507-514","source":"Crossref","is-referenced-by-count":199,"title":["Inhibition of Endogenous TGF-\u03b2 During Experimental Osteoarthritis Prevents Osteophyte Formation and Impairs Cartilage Repair"],"prefix":"10.1093","volume":"169","author":[{"given":"Alwin","family":"Scharstuhl","sequence":"first","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harrie L","family":"Glansbeek","sequence":"additional","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henk M","family":"van Beuningen","sequence":"additional","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elly L","family":"Vitters","sequence":"additional","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter M","family":"van der Kraan","sequence":"additional","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wim B","family":"van den Berg","sequence":"additional","affiliation":[{"name":"Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center , Nijmegen ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,7,1]]},"reference":[{"key":"2026020208173510500_R1","first-page":"190","volume-title":"Stem Cells","year":"1997"},{"key":"2026020208173510500_R2","first-page":"341","volume-title":"Nature","year":"1994"},{"key":"2026020208173510500_R3","first-page":"20172","volume-title":"J. 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