Supplementary Materials

Supplementary Material for:

Neutrophil transfer of miR-223 to lung epithelial cells dampens acute lung injury in mice

Viola Neudecker,* Kelley S. Brodsky, Eric T. Clambey, Eric P. Schmidt, Thomas A. Packard, Bennett Davenport, Theodore J. Standiford, Tingting Weng, Ashley A. Fletcher, Lea Barthel, Joanne C. Masterson, Glenn T. Furuta, Chunyan Cai, Michael R. Blackburn, Adit A. Ginde, Michael W. Graner, William J. Janssen, Rachel L. Zemans, Christopher M. Evans, Ellen L. Burnham, Dirk Homann, Marc Moss, Simone Kreth, Kai Zacharowski, Peter M. Henson, Holger K. Eltzschig

*Corresponding author. Email: viola.neudecker{at}med.uni-muenchen.de

Published 20 September 2017, Sci. Transl. Med. 9, eaah5360 (2017)
DOI: 10.1126/scitranslmed.aah5360

This PDF file includes:

  • Fig. S1. miR-223 expression after coculture and baseline levels of miR-223 (Ct values).
  • Fig. S2. NETosis inhibition and neutrophil-epithelial miRNA transfer detection.
  • Fig. S3. PMN-derived microvesicles in murine BAL fluid and miR-223 in isolated murine pulmonary endothelial cells.
  • Fig. S4. Bone marrow chimera and neutrophil depletion.
  • Fig. S5. miR-223 in macrophages.
  • Fig. S6. Wet–to–dry weight ratios in miR-223−/y mice.
  • Fig. S7. Genetic knockdown of PARP-1 in miR-223−/y mice.
  • Fig. S8. Epithelial cell death in miR-223–overexpressing C57BL/6J mice.
  • Table S1. Significantly down-regulated genes in miR-223–overexpressing epithelial cells.

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