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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Related Experiment Video

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Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
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Fbxw7 controls angiogenesis by regulating endothelial Notch activity.

Nanae Izumi1, Christian Helker, Manuel Ehling

  • 1Max-Planck-Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, Muenster, Germany.

Plos One
|August 1, 2012
PubMed
Summary

Fbxw7 is crucial for blood vessel growth by degrading Notch. Loss of Fbxw7 impairs angiogenesis, increasing Notch activity and hindering vessel development in mice and zebrafish.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Vascular Biology

Background:

  • Notch signaling is essential for blood vessel formation, regulating tip cell selection, proliferation, and differentiation.
  • Fbxw7, an E3 ubiquitin ligase, targets proteins like Notch for degradation, influencing cellular processes.

Purpose of the Study:

  • To investigate the role of Fbxw7 in angiogenesis and its regulation of Notch signaling in endothelial cells.
  • To determine if Fbxw7 acts as a positive or negative regulator of blood vessel growth.

Main Methods:

  • Utilized inducible and endothelial cell-specific Fbxw7 knockout mice (Fbxw7(iECKO)) to study retinal angiogenesis.
  • Employed siRNA knockdown of Fbxw7 in human endothelial cells and morpholino injection in zebrafish embryos.
  • Assessed Notch pathway activity, Dll4 expression, and intersegmental vessel (ISV) sprouting.

Main Results:

  • Fbxw7 deficiency in mice led to impaired retinal blood vessel growth and increased Dll4 expression.
  • Fbxw7 knockdown in human endothelial cells stabilized the active Notch intracellular domain.
  • Fbxw7 inhibition in zebrafish embryos disrupted ISV sprouting, a phenotype reversed by Notch pathway inactivation.

Conclusions:

  • Fbxw7 is a critical positive regulator of angiogenesis, acting by promoting the degradation of active Notch in endothelial cells.
  • The Fbxw7-Notch axis is a key determinant of vascular development and integrity.
  • Targeting Fbxw7 may offer therapeutic strategies for modulating angiogenesis.