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Related Experiment Videos

CD39 modulates endothelial cell activation and apoptosis.

C Goepfert1, M Imai, S Brouard

  • 1Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

Molecular Medicine (Cambridge, Mass.)
|September 21, 2000
PubMed
Summary

CD39 enzyme activity in endothelial cells (ECs) reduces EC activation and apoptosis. This suggests CD39 has vascular protective effects and potential therapeutic applications.

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Area of Science:

  • Biochemistry
  • Vascular Biology
  • Cell Biology

Background:

  • CD39 is a key vascular enzyme hydrolyzing extracellular adenine nucleotides, impacting platelet reactivity.
  • The role of CD39 in endothelial cell (EC) activation and apoptosis was previously unexplored.

Purpose of the Study:

  • To investigate the effects of CD39 on endothelial cell activation and apoptosis.
  • To explore the potential therapeutic applications of CD39 in vascular protection.

Main Methods:

  • Human umbilical vein ECs were infected with recombinant adenoviruses expressing CD39 (rAdCD39) or beta-galactosidase.
  • NTPDase biochemical activity was measured.
  • EC activation, NF-kappaB translocation, E-selectin expression, and apoptosis were assessed.

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Main Results:

  • rAdCD39 infection significantly increased EC NTPDase activity.
  • Elevated CD39 activity inhibited ATP-induced EC activation, including von Willebrand factor secretion and NF-kappaB translocation.
  • CD39 expression reduced ATP-induced E-selectin mRNA transcription and protein synthesis.
  • CD39 attenuated apoptosis triggered by P2X7 receptor activation.

Conclusions:

  • CD39 up-regulation in ECs demonstrates significant vascular protective effects.
  • These findings highlight CD39's potential as a therapeutic target for vascular diseases.