Supplementary Materials

Supplementary Material for:

Recruitment of classical monocytes can be inhibited by disturbing heteromers of neutrophil HNP1 and platelet CCL5

Jean-Eric Alard, Almudena Ortega-Gomez, Kanin Wichapong, Dario Bongiovanni, Michael Horckmans, Remco T. A. Megens, Giovanna Leoni, Bartolo Ferraro, Jan Rossaint, Nicole Paulin, Judy Ng, Hans Ippel, Dennis Suylen, Rabea Hinkel, Xavier Blanchet, Fanny Gaillard, Michele D'Amico, Phillipp von Hundelshausen, Alexander Zarbock, Christoph Scheiermann, Tilman M. Hackeng, Sabine Steffens, Christian Kupatt, Gerry A. F. Nicolaes, Christian Weber, Oliver Soehnlein*

*Corresponding author. E-mail: oliver.soehnlein{at}gmail.com

Published 9 December 2015, Sci. Transl. Med. 7, 317ra196 (2015)
DOI: 10.1126/scitranslmed.aad5330

This PDF file includes:

  • Methods
  • Fig. S1. Secretory products of neutrophils and platelets do not affect adhesion of nonclassical monocytes.
  • Fig. S2. HNP1 and CCL5 stimulate classical monocyte adhesion via CCR5.
  • Fig. S3. CCL5 enables HNP1 to access CCR5.
  • Fig. S4. Design of an HNP1-CCL5 disrupting peptide.
  • Fig. S5. SKY peptide does not affect cell viability.
  • Fig. S6. SKY peptide dose-dependently reduces HNP1-CCL5–mediated monocyte adhesion.
  • Fig. S7. SKY peptide is nonfunctional in the absence of HNP1 and CCL5.
  • Fig. S8. SKY peptide is stable and exerts a long-lasting effect.
  • Fig. S9. SKY peptide inhibits HNP1-CCL5–evoked monocyte adhesion in large arteries.
  • Fig. S10. Presence of neutrophils and platelets after ischemia-reperfusion.
  • Fig. S11. HNP1, CCL5, and the SKY peptide do not affect monocyte homeostasis in myocardial ischemia-reperfusion injury.
  • Fig. S12. Purity of neutrophil and platelet preparations.
  • Table S1. CCL5-binding proteins as identified by mass spectrometry.
  • Legend for table S2
  • Legend for movie S1
  • Reference (40)

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Other Supplementary Material for this manuscript includes the following:

  • Table S2. Source data (Excel).
  • Movie S1 (.mp4 format). Summary of proposed mechanism.