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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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FOXO3 modulates endothelial gene expression and function by classical and alternative mechanisms.

Tobias Czymai1, Dorothee Viemann, Carsten Sticht

  • 1Department of Dermatology, University Medical Center Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany.

The Journal of Biological Chemistry
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FOXO3 transcription factors regulate vascular remodeling via DNA binding, but control cell death independently. BIM and NOXA are key mediators of FOXO3-induced endothelial apoptosis.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • FOXO transcription factors are key regulators of cellular processes, targeted by the PI3K/Akt pathway.
  • Alternative FOXO-dependent gene expression mechanisms beyond DNA binding exist.
  • Understanding these mechanisms is crucial for vascular function.

Purpose of the Study:

  • To investigate the distinct roles of FOXO3 DNA binding and alternative mechanisms in endothelial cells.
  • To elucidate the contribution of FOXO3 to vascular remodeling, cell cycle arrest, and apoptosis.
  • To identify key mediators of FOXO3-induced endothelial apoptosis.

Main Methods:

  • Conditional activation of wild-type FOXO3 and a DNA-binding mutant in human primary endothelial cells.
  • Transcriptional and cellular response analysis.
  • Bioinformatical analysis of co-regulated genes.
  • Molecular analysis of apoptosis pathways, including BCL-2 family members.

Main Results:

  • FOXO3 controls vascular remodeling genes in a DNA-binding-dependent manner.
  • FOXO3-induced cell cycle arrest and apoptosis occur independently of DNA binding.
  • BIM and NOXA are critical mediators of FOXO3-induced endothelial apoptosis, with BIM acting as a cell type-specific mediator and NOXA as an amplifier.

Conclusions:

  • FOXO3 utilizes both DNA-binding-dependent and -independent pathways to regulate endothelial cell function.
  • Alternative FOXO3 regulation is critical for cell cycle arrest and apoptosis.
  • BIM is a key mediator of FOXO3-induced endothelial apoptosis, highlighting its importance in maintaining endothelial integrity.