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Endothelial USP8 is essential for angiogenesis.

Alba Pau-Navalón1,2, Tamara González-Costa1,2, María Lancho Lavilla1

  • 1Intercellular Signalling in Cardiovascular Development and Disease Laboratory CNIC, Centro Nacional de Investigaciones Cardiovasculares Carlos III (F.P.S), Madrid, Spain.

Angiogenesis
|January 28, 2026
PubMed
Summary
This summary is machine-generated.

Endothelial Ubiquitin-Specific Protease 8 (USP8) is vital for blood vessel formation (angiogenesis) during development and after birth. Its absence impairs vascular growth, suggesting USP8 as a therapeutic target for anti-angiogenic treatments.

Keywords:
AngiogenesisDeubiquitinasesUSP8VEGFR2Vessel formation

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Angiogenesis is critical for development and disease, with Vascular Endothelial Growth Factor A (VEGF-A) signaling as a key regulator.
  • Ubiquitin-Specific Protease 8 (USP8) is a deubiquitinase known to influence protein trafficking and activation, including VEGF receptor 2 (VEGFR2) in vitro.
  • Understanding USP8's role in endothelial cells is crucial for developing targeted anti-angiogenic therapies.

Purpose of the Study:

  • To investigate the in vivo function of USP8 in endothelial cells during different developmental and postnatal stages.
  • To elucidate the molecular mechanisms by which USP8 regulates angiogenesis.

Main Methods:

  • Conditional mouse genetics were employed to delete Usp8 in endothelial cells at embryonic, early postnatal, and adult stages.
  • Vascular phenotypes were assessed, including intersomitic vessel formation, retinal angiogenesis, and brain vasculature.
  • Molecular analyses focused on VEGFR2 trafficking, endothelial cell-cycle activation, and signaling pathways like ERK.

Main Results:

  • Endothelial-specific deletion of Usp8 during embryogenesis led to impaired angiogenesis and embryonic lethality.
  • Postnatal deletion caused severe defects in retinal and brain angiogenesis, while adult deletion showed no significant vascular effects.
  • Loss of USP8 resulted in VEGFR2 accumulation in endosomes, reduced cell-cycle activation, and impaired signaling pathways.

Conclusions:

  • Endothelial USP8 is essential for angiogenesis during embryonic and early postnatal development but not for adult vascular homeostasis.
  • USP8 regulates angiogenesis by controlling VEGFR2 trafficking and downstream signaling.
  • USP8 represents a potential therapeutic target for anti-angiogenic strategies in diseases driven by aberrant blood vessel formation.