Myostatin-induced mechanisms of inflammatory bone and cartilage destruction by invasive fibroblast-like synoviocytes

    To investigate the role of myostatin in inflammatory destruction of tissue barriers, we will compare the effects of myostatin deficiency and phamacological inhibition on joint destruction in three arthritis models (different TNF-dependent). In addition, fibroblast-specific myostatin and activin wil be investigated by using Col1α2-Cre mice. Moreover, we want to evaluate the involvement of myostatin/ activin-mediated Smad2 signaling on synovial fibroblast-mediated matrix degradation by investigating proliferation, migration, apoptosis, invasive capacity, adhesion molecules, matrix-degrading proteases as well as involved signaling pathways.

    Research area: Synovial inflammation

    Dr. rer. nat. Berno Dankbar
    Prof. Dr. med. Thomas Pap

    Funding period: July 2016 - June 2020

    • Publications

      Original articles

      • Wehmeyer C, Frank S, Beckmann D, Böttcher M, Cromme C, König U, Fennen M, Held A, Paruzel P, Hartmann C, Stratis A, Korb-Pap A, Kamradt T, Kramer I, van den Berg W, Kneissel M, Pap T, Dankbar B (2016) Sclerostin inhibition promotes TNF-dependent inflammatory joint destruction.  Sci Transl Med. 16;8(330):330ra35.
      • Dankbar B, Fennen M, Brunert D, Hayer S, Frank S, Wehmeyer C, Beckmann D, Paruzel P, Bertrand J, Redlich K, Koers-Wunrau C, Stratis A, Korb-Pap A, Pap T (2015). Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice.  Nat Med. 21(9):1085-90.


      • Fennen M, Pap T, Dankbar B (2016). Smad-dependent mechanisms of inflammatory bone destruction. Arthritis Res Ther. 18: 279-88.