Supplementary Materials

Supplementary Material for:

Neutrophil-derived microvesicles enter cartilage and protect the joint in inflammatory arthritis

Sarah E. Headland, Hefin R. Jones, Lucy V. Norling, Andrew Kim, Patricia R. Souza, Elisa Corsiero, Cristiane D. Gil, Alessandra Nerviani, Francesco Dell'Accio, Costantino Pitzalis, Sonia M. Oliani, Lily Y. Jan, Mauro Perretti*

*Corresponding author. E-mail: m.perretti{at}

Published 25 November 2015, Sci. Transl. Med. 7, 315ra190 (2015)
DOI: 10.1126/scitranslmed.aac5608

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Tmem16f knockout mice have reduced MV shedding and exacerbated sGAG loss in experimental arthritis.
  • Fig. S2. Characterization of parent neutrophils used to generate offspring MVs.
  • Fig. S3. Presence of tetraspanin TSG101 in neutrophil MVs.
  • Fig. S4. Concentration-dependent chondroprotection of MV against cytokine stimulation of chondrocytes.
  • Fig. S5. Selective effect of MV treatment on chondrocyte matrix degrading enzyme mRNA expression.
  • Fig. S6. MV treatment protects from chondrocyte apoptosis.
  • Fig. S7. MV chemokine receptor and adhesion molecule expression.
  • Fig. S8. Neutrophils induce ECM accumulation in chondrocytes only when prohibited from direct cell-to-cell contact.
  • Fig. S9. Generation of neutrophil MVs from AnxA1−/− mice.
  • Table S1. RA patient demographics.
  • Table S2. RA patient clinical profiles.
  • Table S3. RA patient treatment history.
  • Legend for movie S1

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Other Supplementary Material for this manuscript includes the following:

  • Movie S1 (.avi format). MVs penetrate cartilage ex vivo to deliver AnxA1.