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Regulation of angiogenesis by tissue factor cytoplasmic domain signaling

Academic Article
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Overview

authors

  • Belting, M.
  • Dorrell, Michael
  • Sandgren, S.
  • Aguilar, E.
  • Ahamed, J.
  • Dorfleutner, A.
  • Carmeliet, P.
  • Mueller, B. M.
  • Friedlander, Martin
  • Ruf, Wolfram

publication date

  • May 2004

journal

  • Nature Medicine  Journal

abstract

  • Hemostasis initiates angiogenesis-dependent wound healing, and thrombosis is frequently associated with advanced cancer. Although activation of coagulation generates potent regulators of angiogenesis, little is known about how this pathway supports angiogenesis in vivo. Here we show that the tissue factor (TF)-VIIa protease complex, independent of triggering coagulation, can promote tumor and developmental angiogenesis through protease-activated receptor-2 (PAR-2) signaling. In this context, the TF cytoplasmic domain negatively regulates PAR-2 signaling. Mice from which the TF cytoplasmic domain has been deleted (TF Delta CT mice) show enhanced PAR-2-dependent angiogenesis, in synergy with platelet-derived growth factor BB (PDGF-BB). Ocular tissue from diabetic patients shows PAR-2 colocalization with phosphorylated TF specifically on neovasculature, suggesting that phosphorylation of the TF cytoplasmic domain releases its negative regulatory control of PAR-2 signaling in angiogenesis. Targeting the TF-VIIa signaling pathway may thus enhance the efficacy of angiostatic treatments for cancer and neovascular eye diseases.

subject areas

  • Animals
  • Aorta
  • Eye Diseases
  • Humans
  • In Vitro Techniques
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neovascularization, Pathologic
  • Neovascularization, Physiologic
  • Phosphorylation
  • Protein Structure, Tertiary
  • Receptor, PAR-2
  • Signal Transduction
  • Thromboplastin
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Identity

International Standard Serial Number (ISSN)

  • 1078-8956

Digital Object Identifier (DOI)

  • 10.1038/nm1037

PubMed ID

  • 15098027
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Additional Document Info

start page

  • 502

end page

  • 509

volume

  • 10

issue

  • 5

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