{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T19:58:01Z","timestamp":1792699081929,"version":"4.5.0"},"reference-count":47,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2009,2,26]],"date-time":"2009-02-26T00:00:00Z","timestamp":1235606400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2009,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The differentiation of mesenchymal stem cells (MSCs) into chondrocytes provides an attractive basis for the repair and regeneration of articular cartilage. Under clinical conditions, chondrogenesis will often need to occur in the presence of mediators of inflammation produced in response to injury or disease. The purpose of this study was to examine the effects of 2 important inflammatory cytokines, interleukin\u20101\u03b2 (IL\u20101\u03b2) and tumor necrosis factor \u03b1 (TNF\u03b1), on the chondrogenic behavior of human MSCs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Aggregate cultures of MSCs recovered from the femoral intermedullary canal were used. Chondrogenesis was assessed by the expression of relevant transcripts by quantitative reverse transcription\u2013polymerase chain reaction analysis and examination of aggregates by histologic and immunohistochemical analyses. The possible involvement of NF\u2010\u03baB in mediating the effects of IL\u20101\u03b2 was examined by delivering a luciferase reporter construct and a dominant\u2010negative inhibitor of NF\u2010\u03baB (suppressor\u2010repressor form of I\u03baB [srI\u03baB]) with adenovirus vectors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Both IL\u20101\u03b2 and TNF\u03b1 inhibited chondrogenesis in a dose\u2010dependent manner. This was associated with a marked activation of NF\u2010\u03baB. Delivery of srI\u03baB abrogated the activation of NF\u2010\u03baB and rescued the chondrogenic response. Although expression of type X collagen followed this pattern, other markers of hypertrophic differentiation responded differently. Matrix metalloproteinase 13 was induced by IL\u20101\u03b2 in a NF\u2010\u03baB\u2013dependent manner. Alkaline phosphatase activity, in contrast, was inhibited by IL\u20101\u03b2 regardless of srI\u03baB delivery.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Cell\u2010based repair of lesions in articular cartilage will be compromised in inflamed joints. Strategies for enabling repair under these conditions include the use of specific antagonists of individual pyrogens, such as IL\u20101\u03b2 and TNF\u03b1, or the targeting of important intracellular mediators, such as NF\u2010\u03baB.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.24352","type":"journal-article","created":{"date-parts":[[2009,2,26]],"date-time":"2009-02-26T08:15:27Z","timestamp":1235636127000},"page":"801-812","source":"Crossref","is-referenced-by-count":236,"title":["Interleukin\u20101\u03b2 and tumor necrosis factor \u03b1 inhibit chondrogenesis by human mesenchymal stem cells through NF\u2010\u03baB\u2013dependent pathways"],"prefix":"10.1002","volume":"60","author":[{"given":"N.","family":"Wehling","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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