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Endothelial RAF1/ERK activation regulates arterial morphogenesis.

Yong Deng1, Bruno Larrivée, Zhen W Zhuang

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

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|March 27, 2013
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Summary

Endothelial RAF1/ERK pathway activation drives embryonic arterial development and patterning. RAF1 Ser259 phosphorylation is key to preventing excessive pathway activation, ensuring proper vascular formation.

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Area of Science:

  • Vascular Biology
  • Embryonic Development
  • Cell Signaling

Background:

  • Arterial morphogenesis is crucial for embryonic vascular development.
  • Notch signaling primarily controls arterial fate, but guidance factors modulate arterial-venous patterning.
  • Regulation of these pathways remains largely unknown.

Purpose of the Study:

  • To investigate the role of the RAF1/extracellular signal-regulated kinase (ERK) pathway in endothelial cells.
  • To elucidate how this pathway regulates arterial morphogenesis and arterial-venous patterning.

Main Methods:

  • Utilized a constitutively active RAF1 mutant (RAF1 Ser259Ala) resistant to inhibitory phosphorylation.
  • Introduced the mutant into endothelial cells in vitro and in vivo (embryonic development).
  • Assessed embryonic arteriogenic program activation, semaphorin signaling, and arterial-venous patterning.

Main Results:

  • In vitro, RAF1(S259A) induced the embryonic arteriogenic program and semaphorin 6A-dependent cell repulsion.
  • In vivo, endothelial-specific RAF1(S259A) expression promoted extensive arterial morphogenesis in the yolk sac and embryo proper.
  • Disruption of arterial-venous patterning was observed with RAF1(S259A) expression.

Conclusions:

  • Endothelial ERK signaling is critical for both arteriogenesis and arterial-venous patterning.
  • RAF1 Ser259 phosphorylation is essential for preventing unopposed ERK activation during vascular development.