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A Method for Labeling Vasculature in Embryonic Mice
09:58

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Published on: October 7, 2011

ETS factors regulate Vegf-dependent arterial specification.

Joshua D Wythe1, Lan T H Dang, W Patrick Devine

  • 1Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA. jwythe@gladstone.ucsf.edu

Developmental Cell
|July 9, 2013
PubMed
Summary
This summary is machine-generated.

Vascular endothelial growth factor (VEGF) signaling initiates arterial development by activating E26 transformation-specific sequence (ETS) factors, driving Delta-like 4 (Dll4) expression. This pathway specifies arterial identity and Notch signaling in developing blood vessels.

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Area of Science:

  • Developmental biology
  • Molecular biology
  • Cell signaling

Background:

  • Vascular endothelial growth factor (VEGF) signaling is crucial for specifying arterial fate during vascular development.
  • Delta-like 4 (Dll4) is an early Notch ligand gene expressed in arterial precursor cells, but the factors controlling its arterial-specific expression are unknown.

Purpose of the Study:

  • To identify the transcriptional program responsible for initiating arterial Dll4 expression.
  • To elucidate the role of VEGF and Notch signaling in arterial specification.

Main Methods:

  • Characterization of an arterial-specific and VEGF-responsive enhancer of Dll4.
  • Analysis of the role of MAP kinase (MAPK) and E26 transformation-specific sequence (ETS) factors in Dll4 regulation.

Main Results:

  • Notch signaling is not required for the initiation of Dll4 expression in arteries; it acts as a maintenance factor.
  • VEGF signaling activates MAPK-dependent ETS factors in the arterial endothelium.
  • This pathway drives the expression of Dll4 and Notch4, specifying arterial identity.

Conclusions:

  • A novel VEGF/MAPK-dependent transcriptional pathway initiates arterial Dll4 expression.
  • This pathway specifies arterial identity by activating Notch signaling components.
  • Signaling cascades modulate transcription factors for tissue-specific outputs in vascular development.