Supplementary Materials

Supplementary Material for:

Sclerostin inhibition promotes TNF-dependent inflammatory joint destruction

Corinna Wehmeyer, Svetlana Frank, Denise Beckmann, Martin Böttcher, Christoph Cromme, Ulrich König, Michelle Fennen, Annelena Held, Peter Paruzel, Christine Hartmann, Athanasios Stratis, Adelheid Korb-Pap, Thomas Kamradt, Ina Kramer, Wim van den Berg, Michaela Kneissel, Thomas Pap,* Berno Dankbar

*Corresponding author. E-mail: thomas.pap{at}uni-muenster.de

Published 16 March 2016, Sci. Transl. Med. 8, 330ra35 (2016)
DOI: 10.1126/scitranslmed.aac4351

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Sclerostin expression in hind paws of mice with experimental arthritis.
  • Fig. S2. Presence of immune cells in hind paw joints of hTNFtg compared with those of Sost−/−/TNFtgmice.
  • Fig. S3. Anti-sclerostin treatment promotes pannus formation and joint destruction in hTNFtg mice.
  • Fig. S4. Sclerostin inhibits ERK and reduces NF-κB activation.
  • Fig. S5. Sclerostin has no impact on osteoclastogenesis.
  • Fig. S6. Sclerostin also inhibits human TNF-mediated p38 activation.
  • Fig. S7. Sclerostin does not bind to TNF or TNFR and does not influence TNFR shedding and internalization.

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