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Related Experiment Videos

Vascular endothelial growth factor-induced endothelial cell migration and proliferation depend on a nitric

Y Shizukuda1, S Tang, R Yokota

  • 1Cardiovascular Division, Department of Medicine, Department of Molecular Pharmacology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, USA.

Circulation Research
|August 7, 1999
PubMed
Summary

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Vascular endothelial growth factor (VEGF) suppresses Protein Kinase C delta (PKCδ) activity via nitric oxide (NO) signaling. This suppression is essential for VEGF-induced endothelial cell migration and proliferation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Vascular endothelial growth factor (VEGF) stimulates angiogenesis, endothelial cell (EC) migration, and proliferation.
  • Protein Kinase C (PKC) is involved in VEGF signaling, but the roles of specific PKC isoenzymes remain unclear.

Purpose of the Study:

  • To investigate the role of specific PKC isoenzymes in human EC migration and proliferation stimulated by VEGF.
  • To elucidate the signaling pathways involved in VEGF-induced PKC isoenzyme modulation.

Main Methods:

  • Assessed PKC isoenzyme activity in human umbilical vein ECs (HUVECs) and an EC line (ECV) following VEGF stimulation.
  • Utilized nitric oxide (NO) synthase inhibitors and NO donors to investigate the involvement of NO in VEGF signaling.
  • Examined the effects of PKCδ overexpression on EC responses to VEGF, FGF-2, and serum.

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Main Results:

  • VEGF stimulation significantly decreased PKCδ specific activity in HUVECs and ECV cells without altering total protein or mRNA levels.
  • The VEGF-induced reduction in PKCδ activity was blocked by a nitric oxide synthase inhibitor and mimicked by an exogenous NO donor.
  • Inhibition of NO synthase blocked VEGF-induced EC migration and proliferation, while FGF-2 and serum-induced responses remained unaffected.
  • Overexpression of PKCδ specifically inhibited EC responses to VEGF but not to FGF-2 or serum.

Conclusions:

  • Suppression of PKCδ activity through a nitric oxide synthase-dependent pathway is a critical requirement for VEGF-induced endothelial cell migration and proliferation.
  • This mechanism is specific to VEGF signaling and does not appear to mediate responses induced by FGF-2 or serum.