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WNT7b mediates macrophage-induced programmed cell death in patterning of the vasculature

Author

Listed:
  • Ivan B. Lobov

    (University of Cincinnati
    Regeneron Pharmaceuticals)

  • Sujata Rao

    (University of Cincinnati)

  • Thomas J. Carroll

    (Harvard University
    University of Texas Southwestern Medical Center at Dallas)

  • Jefferson E. Vallance

    (University of Cincinnati)

  • Masataka Ito

    (National Defense Medical College)

  • Jennifer K. Ondr

    (University of Cincinnati)

  • Savita Kurup

    (University of Cincinnati
    University of Sydney)

  • Donald A. Glass

    (Baylor College of Medicine)

  • Millan S. Patel

    (Baylor College of Medicine)

  • Weiguo Shu

    (University of Pennsylvania)

  • Edward E. Morrisey

    (University of Pennsylvania)

  • Andrew P. McMahon

    (Harvard University)

  • Gerard Karsenty

    (Baylor College of Medicine)

  • Richard A. Lang

    (University of Cincinnati)

Abstract

Macrophages have a critical role in inflammatory and immune responses through their ability to recognize and engulf apoptotic cells1. Here we show that macrophages initiate a cell-death programme in target cells by activating the canonical WNT pathway. We show in mice that macrophage WNT7b is a short-range paracrine signal required for WNT-pathway responses and programmed cell death in the vascular endothelial cells of the temporary hyaloid vessels of the developing eye. These findings indicate that macrophages can use WNT ligands to influence cell-fate decisions—including cell death—in adjacent cells, and raise the possibility that they do so in many different cellular contexts.

Suggested Citation

  • Ivan B. Lobov & Sujata Rao & Thomas J. Carroll & Jefferson E. Vallance & Masataka Ito & Jennifer K. Ondr & Savita Kurup & Donald A. Glass & Millan S. Patel & Weiguo Shu & Edward E. Morrisey & Andrew P, 2005. "WNT7b mediates macrophage-induced programmed cell death in patterning of the vasculature," Nature, Nature, vol. 437(7057), pages 417-421, September.
    • Handle: RePEc:nat:nature:v:437:y:2005:i:7057:d:10.1038_nature03928
    DOI: 10.1038/nature03928
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