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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...
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The development of the vascular system in a fetus is a complex and intricate process that begins as early as 15 to 16 days post-conception. This process starts outside the embryo, specifically in the mesoderm of the yolk sac, chorion, and connecting stalk. Approximately two days later, the formation of blood vessels occurs within the embryo itself.
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Updated: Jul 26, 2025

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PRDM16 regulates arterial development and vascular integrity.

Michael Thompson1,2, Masahide Sakabe1,2, Mark Verba1,2

  • 1Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.

Frontiers in Physiology
|June 16, 2023
PubMed
Summary

PRDM16 maintains arterial endothelial cell identity by suppressing venous markers and promoting vascular smooth muscle cell recruitment. This transcription factor is crucial for arterial development and function.

Keywords:
PRDM16angiogenesisangiopoietinarteryvascular development

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Area of Science:

  • Vascular Biology
  • Cellular and Molecular Biology
  • Developmental Biology

Background:

  • Vascular formation relies on signaling pathways like VEGF and Notch.
  • Mechanisms maintaining arterial endothelial cell characteristics are not fully understood.

Purpose of the Study:

  • Investigate the role of PRDM16 in maintaining arterial endothelial cell identity.

Main Methods:

  • Assessed PRDM16 expression in developing embryos and neonatal retinas.
  • Performed endothelial-specific deletion of Prdm16 in mice.
  • Conducted whole-genome transcriptome analysis on isolated brain endothelial cells.
  • Forced PRDM16 expression in venous endothelial cells.

Main Results:

  • PRDM16 is expressed in arterial ECs but not venous ECs.
  • Prdm16 deletion induced venous markers in arterial ECs and reduced vSMC recruitment.
  • Prdm16 knockout upregulated Angpt2 expression, inhibiting vSMC recruitment.
  • Forced PRDM16 expression in venous ECs induced arterial genes and repressed ANGPT2.

Conclusions:

  • PRDM16 functions autonomously in arterial ECs to suppress venous characteristics.
  • PRDM16 is essential for maintaining arterial identity and regulating vSMC interactions.