TGF β-induced cartilage repair is maintained but fibrosis is blocked in the presence of Smad7

摘要: Cartilage damage in osteoarthritis (OA) is considered an imbalance between catabolic and anabolic factors, favoring the side. We assessed whether adenoviral overexpression of transforming growth factor-β (TGFβ) enhanced cartilage repair TGFβ-induced fibrosis was blocked by local expression intracellular TGFβ inhibitor Smad7. inflicted injection interleukin-1 (IL-1) into murine knee joints. After 2 days, we injected adenovirus encoding TGFβ. On day 4, measured proteoglycan (PG) synthesis content. To examine could block stimulate simultaneously, Ad-TGFβ Ad-Smad7. This performed both after IL-1-induced a model primary OA. In addition to PG cartilage, synovial determining width number procollagen I-expressing cells. Adenoviral restored reduction content increased synthesis. elevation OA model. strongly diminished simultaneous Smad7 lining. Of great interest, did not reduce repair-stimulating effect on cartilage. stimulated IL-1- OA-damaged locally inhibiting signaling lining simultaneously transfecting it with overexpressing