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Angiogenic factor-driven inflammation promotes extravasation of human proangiogenic monocytes to tumours

Author

Listed:
  • Adama Sidibe

    (University of Geneva
    Centre Médical Universitaire (CMU), Medical faculty, University of Geneva)

  • Patricia Ropraz

    (University of Geneva)

  • Stéphane Jemelin

    (University of Geneva)

  • Yalin Emre

    (University of Geneva)

  • Marine Poittevin

    (University of Geneva)

  • Marc Pocard

    (Hospital Lariboisière
    Université Paris Diderot, Sorbonne Paris Cité, CART, INSERM U965)

  • Paul F. Bradfield

    (University of Geneva)

  • Beat A. Imhof

    (University of Geneva)

Abstract

Recruitment of circulating monocytes is critical for tumour angiogenesis. However, how human monocyte subpopulations extravasate to tumours is unclear. Here we show mechanisms of extravasation of human CD14dimCD16+ patrolling and CD14+CD16+ intermediate proangiogenic monocytes (HPMo), using human tumour xenograft models and live imaging of transmigration. IFNγ promotes an increase of the chemokine CX3CL1 on vessel lumen, imposing continuous crawling to HPMo and making these monocytes insensitive to chemokines required for their extravasation. Expression of the angiogenic factor VEGF and the inflammatory cytokine TNF by tumour cells enables HPMo extravasation by inducing GATA3-mediated repression of CX3CL1 expression. Recruited HPMo boosts angiogenesis by secreting MMP9 leading to release of matrix-bound VEGF-A, which amplifies the entry of more HPMo into tumours. Uncovering the extravasation cascade of HPMo sets the stage for future tumour therapies.

Suggested Citation

  • Adama Sidibe & Patricia Ropraz & Stéphane Jemelin & Yalin Emre & Marine Poittevin & Marc Pocard & Paul F. Bradfield & Beat A. Imhof, 2018. "Angiogenic factor-driven inflammation promotes extravasation of human proangiogenic monocytes to tumours," Nature Communications, Nature, vol. 9(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02610-0
    DOI: 10.1038/s41467-017-02610-0
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