Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

PMA-activated neutrophils decrease pulmonary endothelial ectoenzyme activities in perfused rabbit lungs.

X Chen1, J D Catravas

  • 1Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912-2300.

The American Journal of Physiology
|December 1, 1992
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G<sup>+</sup>-bacterial toxins.

Biochemical pharmacology·2016
Same author

Regulation of asthmatic airway relaxation by estrogen and heat shock protein 90.

Journal of cellular physiology·2011
Same author

Pulmonary capillary endothelial metabolic function in chronic thromboembolic pulmonary hypertension.

Journal of thrombosis and haemostasis : JTH·2008
Same author

Functional significance of hsp90 complexes with NOS and sGC in endothelial cells.

Clinical hemorheology and microcirculation·2007
Same author

Angiotensin, bradykinin and the endothelium.

Handbook of experimental pharmacology·2006
Same author

Quantification of pulmonary capillary endothelium-bound angiotensin converting enzyme inhibition in man.

General pharmacology·2002
Same journal

Blood coagulation in fish.

The American journal of physiology·2011
Same journal

Renal tubular reabsorption, metabolic utilization and isomeric fractionation of lactic acid in the dog.

The American journal of physiology·2010
Same journal

The inactivation of placental toxin by human serum.

The American journal of physiology·2010
Same journal

Adrenal function following ovariectomy in the rat.

The American journal of physiology·2010
Same journal

Capillary permeability; perfusion of frog and guinea pig hind limbs.

The American journal of physiology·2010
Same journal

Evaluation of protective measures against sunburn.

The American journal of physiology·2010
See all related articles

Phorbol 12-myristate 13-acetate (PMA) activates neutrophils, impairing pulmonary angiotensin-converting enzyme (ACE) and 5'-nucleotidase (NCT) function. This study reveals how activated neutrophils impact lung ectoenzyme activity.

Area of Science:

  • Pulmonary physiology
  • Endothelial cell biology
  • Enzymology

Background:

  • Pulmonary endothelial ectoenzymes, such as angiotensin-converting enzyme (ACE) and 5 -nucleotidase (NCT), play critical roles in regulating vascular tone and lung function.
  • Phorbol 12-myristate 13-acetate (PMA) is a potent activator of neutrophils, which can release inflammatory mediators and enzymes.
  • The impact of PMA-activated neutrophils on pulmonary ectoenzyme function remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of PMA-activated neutrophils on the function of pulmonary endothelial ectoenzymes, specifically ACE and NCT.
  • To determine how neutrophil activation by PMA influences the catalytic activity and kinetic parameters of these enzymes in isolated rabbit lungs.

Main Methods:

  • Isolated rabbit lungs were perfused with either platelet-poor plasma (PPP) or platelet-rich plasma (PRP).

Related Experiment Videos

  • Lungs were treated with phorbol 12-myristate 13-acetate (PMA) in the presence or absence of neutrophils.
  • Enzyme activities of ACE and NCT were assessed using indicator-dilution techniques by measuring substrate hydrolysis ([3H]benzoyl-Phe-Ala-Pro for ACE and 14C-labeled AMP for NCT).

    • Main Results:

    • PMA induced a delayed increase in pulmonary vascular resistance across all treatment groups.
    • PMA-activated neutrophils significantly decreased the percent metabolism (%M) of the ACE substrate ([3H]BPAP).
    • Activated neutrophils reduced the apparent first-order parameter (Amax/Km) for ACE and increased the Km values for both ACE and NCT, while Amax remained unchanged.

    Conclusions:

    • PMA-activated neutrophils impair the function of pulmonary endothelial ACE and NCT.
    • The observed changes in enzyme kinetics suggest altered substrate affinity rather than changes in enzyme mass or microvascular surface area.
    • These findings highlight a potential mechanism by which inflammatory cells can modulate lung endothelial enzyme activity, impacting pulmonary physiology.