Laminin-Binding Integrins Induce Dll4 Expression and Notch Signaling in Endothelial Cells

@article{Estrach2011LamininBindingII,
  title={Laminin-Binding Integrins Induce Dll4 Expression and Notch Signaling in Endothelial Cells},
  author={Soline Estrach and Laurence Cailleteau and Cl{\'a}udio A. Franco and Holger Gerhardt and Caroline Stefani and Emmanuel Lemichez and Laurent Gagnoux-Palacios and Guerrino Meneguzzi and Amel Mettouchi},
  journal={Circulation Research},
  year={2011},
  volume={109},
  pages={172–182}
}
Rationale: Integrins play a crucial role in controlling endothelial cell proliferation and migration during angiogenesis. The Delta-like 4 (Dll4)/Notch pathway establishes an adequate ratio between stalk and tip cell populations by restricting tip cell formation through “lateral inhibition” in response to a vascular endothelial growth factor gradient. Because angiogenesis requires a tight coordination of these cellular processes, we hypothesized that adhesion, vascular endothelial growth factor… 
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TLDR
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TLDR
It is shown here that vascular endothelial growth factor but not basic fibroblast growth factor can induce gene expression of Notch1 and its ligand, Delta-like 4 (Dll4), in human arterial endothelial cells.
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TLDR
The findings suggest that constitutive Notch4 activation in endothelial cells inhibits angiogenesis in part by promoting β1-integrin-mediated adhesion to the underlying matrix.
Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis
TLDR
Evidence is presented that delta-like 4 (Dll4)–Notch1 signalling regulates the formation of appropriate numbers of tip cells to control vessel sprouting and branching in the mouse retina, and modulators of Dll4 or Notch signalling, such as γ-secretase inhibitors developed for Alzheimer's disease, might find usage as pharmacological regulators of angiogenesis.
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TLDR
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TLDR
Dll4 is revealed as a negative regulator of vascular sprouting and vessel branching that is required for normal vascular network formation during development by inhibiting endothelial tip cell formation.
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TLDR
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TLDR
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