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FGF-dependent regulation of VEGF receptor 2 expression in mice

Masahiro Murakami1, Loc T Nguyen, Kunihiko Hatanaka

  • 1Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.

The Journal of Clinical Investigation
|June 3, 2011
PubMed

Insights

Fibroblast Growth Factor (FGF) signaling is crucial for maintaining Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) expression in endothelial cells. This ensures proper response to VEGF, vital for blood vessel formation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Vascular Biology

Background:

  • The relationship between Fibroblast Growth Factor (FGF) and Vascular Endothelial Growth Factor (VEGF) signaling pathways in angiogenesis remains unclear.
  • Understanding this link is essential for elucidating mechanisms of vascular development and integrity.

Purpose of the Study:

  • To investigate the role of FGF signaling in regulating VEGF signaling in endothelial cells (ECs).
  • To determine the molecular mechanisms by which FGF influences VEGF receptor expression and function.

Main Methods:

  • In vitro studies using ECs with disrupted FGF signaling.
  • In vivo experiments in mouse models with defective FGF signaling.
  • Analysis of VEGF receptor 2 (VEGFR2) expression, enhancer activation, Erk1/2 signaling, and Ets transcription factor activity.

Main Results:

  • Disruption of FGF signaling rendered ECs unresponsive to VEGF due to decreased VEGFR2 expression.
  • FGF signaling mediated VEGFR2 expression via Erk1/2 activation and Ets transcription factors.
  • Mice with impaired FGF signaling showed compromised vascular integrity and morphogenesis.

Conclusions:

  • Basal FGF stimulation of the endothelium is necessary for maintaining VEGFR2 expression.
  • FGF signaling is required for endothelial cells to respond to VEGF, establishing a hierarchical control in vascular formation.
  • This study clarifies the interplay between FGF and VEGF pathways in regulating angiogenesis.

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