tailieunhanh - Báo cáo y học: " TGF β-induced cartilage repair is maintained but fibrosis is blocked in the presence of Smad7"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: TGF β-induced cartilage repair is maintained but fibrosis is blocked in the presence of Smad7. | Available online http content 8 3 R65 Research article TGF p-induced cartilage repair is maintained but fibrosis is blocked in the presence of Smad7 Esmeralda N Blaney Davidson Elly L Vitters Wim B van den Berg and Peter M van der Kraan Experimental Rheumatology and Advanced Therapeutics St. Radboud University Medical Centre Nijmegen Geert Grooteplein 26-28 6525 GA Nijmegen The Netherlands Corresponding author Esmeralda N Blaney Davidson Received 9 Jan 2006 Revisions requested 3 Feb 2006 Revisions received 23 Feb 2006 Accepted 7 Mar 2006 Published 29 Mar 2006 Arthritis Research Therapy 2006 8 R65 doi ar1 931 This article is online at http content 8 3 R65 2006 Blaney Davidson et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Cartilage damage in osteoarthritis OA is considered an imbalance between catabolic and anabolic factors favoring the catabolic side. We assessed whether adenoviral overexpression of transforming growth factor-p TGFp enhanced cartilage repair and whether TGFp-induced fibrosis was blocked by local expression of the intracellular TGFp inhibitor Smad7. We inflicted cartilage damage by injection of interleukin-1 IL-1 into murine knee joints. After 2 days we injected an adenovirus encoding TGFp. On day 4 we measured proteoglycan PG synthesis and content. To examine whether we could block TGFp-induced fibrosis and stimulate cartilage repair simultaneously we injected Ad-TGFp and Ad-Smad7. This was performed both after IL-1-induced damage and in a model of primary OA. In addition to PG in cartilage synovial fibrosis was measured by determining the synovial width and the number of procollagen .