Reduced transforming growth factor-beta signaling in cartilage of old mice role in impaired repair capacity 英文参考文献.docVIP

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Reduced transforming growth factor-beta signaling in cartilage of old mice role in impaired repair capacity 英文参考文献.doc

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Reduced transforming growth factor-beta signaling in cartilage of old mice role in impaired repair capacity 英文参考文献

Available online /content/7/6/R1338 Research article Open Access Vol 7 No 6 Reduced transforming growth factor-beta signaling in cartilage of old mice: role in impaired repair capacity EN Blaney Davidson, A Scharstuhl, EL Vitters, PM van der Kraan and WB van den Berg Experimental Rheumatology and Advanced Therapeutics, St Radboud University Medical Centre Nijmegen, Geert Grooteplein 26, 6525 GA Nijmegen, The Netherlands Corresponding author: PM van der Kraan, p.vanderkraan@reuma.umcn.nl Received: 4 Jul 2005 Revisions requested: 26 Jul 2005 Revisions received: 18 Aug 2005 Accepted: 1 Sep 2005 Published: 30 Sep 2005 Arthritis Research Therapy 2005, 7:R1338-R1347 (DOI 10.1186/ar1833) This article is online at: /content/7/6/R1338 ? 2005 Blaney Davidson et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/ 2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Osteoarthritis (OA) is a common joint disease, mainly effecting the elderly population. The cause of OA seems to be an imbalance in catabolic and anabolic factors that develops with age. IL-1 is a catabolic factor known to induce cartilage damage, and transforming growth factor (TGF)-beta is an anabolic factor that can counteract many IL-1-induced effects. In old mice, we observed reduced responsiveness to TGF-beta-induced IL-1 counteraction. We investigated whether expression of TGF-beta and its signaling molecules altered with age. To mimic the TGF- beta deprived conditions in aged mice, we assessed the functional consequence of TGF-beta blocking. We isolated knee joints of mice aged 5 months or 2 years, half of which were exposed to IL-1 by intra-articular injection 24 h prior to knee joint isolation. Immunohistochemistry was performed, staining for TGF-beta1, -2 or -3, TGF-betaRI o