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Related Experiment Videos

CD39 modulates IL-1 release from activated endothelial cells.

M Imai1, C Goepfert, E Kaczmarek

  • 1Department of Surgery, Harvard Medical School, Boston, Massachusetts 02215, USA.

Biochemical and Biophysical Research Communications
|March 29, 2000
PubMed
Summary

Lipopolysaccharide (LPS) triggers ATP release from endothelial cells (EC), leading to Interleukin-1 alpha (IL-1α) release. CD39/nucleoside triphosphate diphosphohydrolase (NTPDase) inhibits this ATP-mediated IL-1α release in EC.

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Area of Science:

  • Vascular biology
  • Immunology
  • Cell signaling

Background:

  • Endothelial cell (EC) and monocyte-macrophage activation by lipopolysaccharide (LPS) contributes to vascular injury in endotoxemia.
  • Interleukin-1 beta (IL-1β) release from macrophages involves ATP release via P2X7 receptor activation.
  • CD39 (nucleoside triphosphate diphosphohydrolase; NTPDase) is highly expressed in EC and may influence nucleotide-mediated signaling.

Purpose of the Study:

  • To investigate whether CD39 modulates ATP-mediated Interleukin-1 (IL-1) release from LPS-stimulated human EC.
  • To elucidate the role of CD39 in the signaling pathway linking LPS, ATP, and IL-1 release in EC.

Main Methods:

  • Human EC were stimulated with LPS.
  • ATP and IL-1α secretion levels were measured.

Related Experiment Videos

  • CD39 was overexpressed using recombinant adenoviral vectors (AdCD39) or by using soluble NTPDase.

    • Main Results:

    • LPS stimulation induced ATP secretion from EC, followed by IL-1α release.
    • Overexpression of CD39 abrogated the initial ATP secretion phase and inhibited IL-1α release.
    • Soluble NTPDase yielded comparable inhibitory results on IL-1α release.

    Conclusions:

    • CD39/NTPDase plays a significant role in modulating IL-1α release from LPS-stimulated human EC.
    • The findings highlight a novel mechanism involving CD39 in regulating inflammatory responses in EC during endotoxemia.