{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:59:24Z","timestamp":1773291564969,"version":"3.50.1"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,12,17]],"date-time":"2007-12-17T00:00:00Z","timestamp":1197849600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Pro\u2010inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro\u2010inflammatory cytokines such as interleukin\u20101\u03b2 (IL\u20101\u03b2) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase\u20101 (HO\u20101) is down\u2010regulated by pro\u2010inflammatory cytokines and up\u2010regulated by IL\u201010 in OA chondrocytes. The aim of this study was to determine whether HO\u20101 can modify the catabolic effects of IL\u20101\u03b2 in OA cartilage and chondrocytes. Up\u2010regulation of HO\u20101 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL\u20101\u03b2 in OA cartilage explants but increased glycosaminoglycan synthesis and the expression of collagen II in OA chondrocytes in primary culture, as determined by radiometric procedures, immunoblotting and immunocytochemistry. HO\u20101 decreased the activation of extracellular signal\u2010regulated kinase 1\/2. This was accompanied by a significant inhibition in MMP activity and expression of collagenases MMP\u20101 and MMP\u201013 at the protein and mRNA levels. In addition, HO\u20101 induction caused a significant increase in the production of insulin\u2010like growth factor\u20101 and a reduction in the levels of insulin\u2010like growth factor binding protein\u20103. We have shown in primary culture of chondrocytes and articular explants from OA patients that HO\u20101 counteracts the catabolic and anti\u2010anabolic effects of IL\u20101\u03b2. Our data thus suggest that HO\u20101 may be a factor regulating the degradation and synthesis of extracellular matrix components in OA. Copyright \u00a9 2008 Pathological Society of Great Britain and Ireland. 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