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Related Experiment Videos

PMA-activated neutrophils decrease ectoenzyme activities in rabbit aortic endothelial cells in culture.

X Chen1, M Tzanela, M K Baumgartner

  • 1Department of Pharmacology, Medical College of Georgia, Augusta.

The American Journal of Physiology
|December 1, 1992
PubMed
Summary
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Phorbol 12-myristate 13-acetate (PMA)-activated neutrophils significantly decrease angiotensin-converting enzyme (ACE) activity in endothelial cells. This effect is dose-dependent and mediated by neutrophil adherence, impacting ectoenzyme function.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Endothelial ectoenzymes, such as angiotensin-converting enzyme (ACE) and 5'-nucleotidase (NCT), play crucial roles in vascular function.
  • Neutrophils, activated by phorbol 12-myristate 13-acetate (PMA), can interact with endothelial cells and potentially modulate their enzymatic activities.

Purpose of the Study:

  • To investigate the impact of PMA-activated neutrophils on the activity of endothelial ACE and NCT.
  • To elucidate the mechanisms underlying these interactions, including the role of neutrophil adherence.

Main Methods:

  • Cultured rabbit aortic endothelial cells (EC) were incubated with PMA-activated neutrophils (PMN).
  • ACE and NCT activities were measured using specific radiolabeled substrates under first-order reaction conditions.

Related Experiment Videos

  • Cytotoxicity was assessed by 51Cr release, and neutrophil adherence was quantified.

    • Main Results:

    • PMA-activated PMN significantly reduced EC ACE activity in a dose-dependent manner, with complete abolition at 8 ng/ml PMA, without causing cytotoxicity.
    • The decrease in ACE activity was also dependent on PMN concentration and occurred rapidly (within 1 hour).
    • PMA alone increased NCT activity, while coincubation with PMN decreased NCT activity (20-29%), independent of PMA and PMN concentrations.

    Conclusions:

    • PMA-activated neutrophils, through adherence mechanisms involving CD18, can significantly inhibit endothelial ACE activity.
    • Neutrophil-endothelial cell interactions can modulate key ectoenzyme functions, suggesting a role in vascularpathophysiology.