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Repulsive guidance molecule A suppresses angiogenesis.

Kana Harada1, Yuki Fujita1, Toshihide Yamashita1

  • 1Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), 5 Sanbancho, Chiyoda-ku, Tokyo, Japan.

Biochemical and Biophysical Research Communications
|January 2, 2016
PubMed
Summary

Repulsive guidance molecule-a (RGMa) inhibits new blood vessel formation. This protein suppresses angiogenesis in vitro and in vivo, offering a potential therapeutic target for conditions with excessive blood vessel growth.

Keywords:
AngiogenesisFocal adhesion kinaseHUAECNeogeninRGM

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Repulsive guidance molecule-a (RGMa) is a glycoprotein with known roles in the central nervous system.
  • Its function in regulating vascularization is not well understood.

Purpose of the Study:

  • To investigate the role of RGMa in angiogenesis.
  • To determine the mechanism by which RGMa affects blood vessel formation.

Main Methods:

  • In vitro studies using human umbilical artery endothelial cells (HUAEC) treated with recombinant RGMa on Matrigel.
  • Assays for tubular formation, migration, and cell adhesion.
  • In vivo Matrigel plug assay to assess angiogenesis.

Main Results:

  • Recombinant RGMa inhibited both vascular endothelial growth factor (VEGF)-induced and VEGF-independent HUAEC tubular formation and migration.
  • RGMa enhanced HUAEC adhesion, likely via dephosphorylation of focal adhesion kinase (FAK) at tyrosine-397.
  • The RGMa receptor, neogenin, was essential for RGMa's effects.
  • In vivo, RGMa treatment suppressed angiogenesis in the Matrigel plug assay.

Conclusions:

  • RGMa acts as an inhibitor of angiogenesis both in vitro and in vivo.
  • RGMa's mechanism involves enhanced cell adhesion through FAK dephosphorylation and requires neogenin.
  • Targeting RGMa could be a therapeutic strategy for diseases characterized by excessive blood vessel formation.