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CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury

Author

Listed:
  • Hirokuni Akahori

    (Emory University)

  • Vinit Karmali

    (Emory University)

  • Rohini Polavarapu

    (Emory University)

  • Alicia N. Lyle

    (Emory University)

  • Daiana Weiss

    (Emory University)

  • Eric Shin

    (Emory University)

  • Ahsan Husain

    (Emory University)

  • Nawazish Naqvi

    (Emory University)

  • Richard Van Dam

    (Emory University)

  • Anwer Habib

    (Emory University)

  • Cheol Ung Choi

    (Emory University
    Cardiovascular Center, Korea University Guro Hospital, Korea University College of Medicine)

  • Adrienne L. King

    (Evolution, and Organismal Biology Kennesaw)

  • Kimberly Pachura

    (Emory University)

  • W. Robert Taylor

    (Emory University
    Atlanta VA Medical Center
    Coulter Department of Biomedical Engineering at Georgia Tech and Emory)

  • David J. Lefer

    (LSU Health Sciences Center, New Orleans)

  • Aloke V. Finn

    (Emory University)

Abstract

Macrophages are an essential component of the immune response to ischaemic injury and play an important role in promoting inflammation and its resolution, which is necessary for tissue repair. The type I transmembrane glycoprotein CD163 is exclusively expressed on macrophages, where it acts as a receptor for haemoglobin:haptoglobin complexes. An extracellular portion of CD163 circulates in the blood as a soluble protein, for which no physiological function has so far been described. Here we show that during ischaemia, soluble CD163 functions as a decoy receptor for TWEAK, a secreted pro-inflammatory cytokine of the tumour necrosis factor family, to regulate TWEAK-induced activation of canonical nuclear factor-κB (NF-κB) and Notch signalling necessary for myogenic progenitor cell proliferation. Mice with deletion of CD163 have transiently elevated levels of TWEAK, which stimulate muscle satellite cell proliferation and tissue regeneration in their ischaemic and non-ischaemic limbs. These results reveal a role for soluble CD163 in regulating muscle regeneration after ischaemic injury.

Suggested Citation

  • Hirokuni Akahori & Vinit Karmali & Rohini Polavarapu & Alicia N. Lyle & Daiana Weiss & Eric Shin & Ahsan Husain & Nawazish Naqvi & Richard Van Dam & Anwer Habib & Cheol Ung Choi & Adrienne L. King & K, 2015. "CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury," Nature Communications, Nature, vol. 6(1), pages 1-14, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8792
    DOI: 10.1038/ncomms8792
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