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Related Experiment Videos

PPACK attenuates plasmin-induced changes in endothelial integrity

L E Rabbani1, M T Johnstone, M A Rudd

  • 1Department of Medicine, Brigham and Women's Hospital, Boston, MA.

Thrombosis Research
|June 15, 1993
PubMed
Summary

Plasmin significantly increases endothelial cell permeability and alters cell morphology. A specific plasmin inhibitor, D-phenylalanyl-L-prolyl-L-arginyl chloromethylketone, effectively reduces these harmful effects on endothelial cells.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Vascular Biology

Background:

  • Endothelial cells form a critical barrier regulating vascular permeability.
  • Plasmin, a serine protease, plays roles in fibrinolysis and extracellular matrix remodeling.
  • The direct impact of plasmin on endothelial cell integrity requires elucidation.

Purpose of the Study:

  • To investigate the direct effects of plasmin on endothelial cell integrity and morphology.
  • To assess the protective role of a plasmin inhibitor against plasmin-induced endothelial damage.

Main Methods:

  • Confluent bovine aortic endothelial cells were treated with plasminogen and a plasminogen activator.
  • Endothelial permeability was measured using [125I]-albumin.
  • Cell morphology was assessed via rhodamine-phalloidin staining for F-actin.

Related Experiment Videos

  • The effect of D-phenylalanyl-L-prolyl-L-arginyl chloromethylketone on plasmin-induced changes was evaluated.

    • Main Results:

    • Plasmin treatment significantly increased endothelial cell permeability and decreased cell viability.
    • A strong positive correlation was observed between plasmin activity and endothelial permeability (r = 0.82).
    • Significant morphologic changes in endothelial monolayers were noted upon plasmin exposure.
    • Coincubation with the plasmin inhibitor D-phenylalanyl-L-prolyl-L-arginyl chloromethylketone reduced permeability increase by 59% and attenuated morphologic alterations.

    Conclusions:

    • Plasmin directly induces significant increases in endothelial cell permeability and causes detrimental morphologic changes.
    • The plasmin inhibitor D-phenylalanyl-L-prolyl-L-arginyl chloromethylketone effectively mitigates these functional and morphologic impairments.
    • These findings highlight plasmin's role in endothelial barrier dysfunction and suggest therapeutic potential for plasmin inhibitors.