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Related Experiment Videos

Upregulation of angiotensin-converting enzyme by vascular endothelial growth factor.

O Saijonmaa1, T Nyman, R Kosonen

  • 1Minerva Institute for Medical Research, Helsinki University Central Hospital, SF-00250 Helsinki, Finland. Outi.Saijonmaa@helsinki.fi

American Journal of Physiology. Heart and Circulatory Physiology
|February 13, 2001
PubMed
Summary

Vascular Endothelial Growth Factor (VEGF) increases Angiotensin-Converting Enzyme (ACE) in endothelial cells, suggesting a link between VEGF and the renin-angiotensin system in vascular health.

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Area of Science:

  • Endothelial biology
  • Vascular signaling
  • Biochemistry

Background:

  • Vascular Endothelial Growth Factor (VEGF) is a key regulator of angiogenesis.
  • Angiotensin-Converting Enzyme (ACE) plays a critical role in the renin-angiotensin system and vascular function.
  • The interplay between VEGF and ACE in endothelial cells is not fully understood.

Purpose of the Study:

  • To investigate the role of VEGF in regulating ACE expression and activity in human umbilical vein endothelial cells (HUVECs).
  • To elucidate the intracellular signaling pathways involved in VEGF-induced ACE regulation.

Main Methods:

  • Cultured HUVECs were treated with varying concentrations of VEGF.
  • ACE activity and mRNA expression were measured.
  • The effects of various inhibitors (tyrosine kinase, cGMP phosphodiesterase, nitric oxide synthase, COX, PKC inhibitors) were assessed.

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  • PKC was downregulated using phorbol esters.

    • Main Results:

    • VEGF significantly increased ACE activity and ACE mRNA expression in HUVECs in a dose-dependent manner.
    • VEGF-induced ACE upregulation was inhibited by a tyrosine kinase inhibitor and a PKC inhibitor.
    • cGMP phosphodiesterase inhibition potentiated VEGF's effect, while nitric oxide synthase inhibition suppressed it.
    • COX-2 inhibition potentiated VEGF's effect, but COX-1 inhibition had no effect.

    Conclusions:

    • VEGF induces ACE expression and activity in cultured HUVECs.
    • Intracellular signaling pathways involving tyrosine kinase, PKC, and cGMP are implicated in VEGF-mediated ACE induction.
    • Nitric oxide may play a partial role in this process.
    • The findings suggest a synergistic relationship between VEGF and the renin-angiotensin system in vascular biology.