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Related Experiment Videos

Plasminogen activator inhibitor-2 expression in inflamed appendix

S A Whawell1, E M Thompson, K A Fleming

  • 1Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London.

Histopathology
|July 1, 1995
PubMed
Summary

Plasminogen activator inhibitor-2 (PAI-2) is found in macrophages of normal appendix tissue. In inflamed tissue, PAI-2 is also produced by mesothelial cells, contributing to fibrin deposition in peritonitis.

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Area of Science:

  • Peritoneal biology
  • Inflammation research
  • Molecular pathology

Background:

  • Plasminogen activator inhibitors (PAIs) reduce fibrinolysis in inflamed peritoneum, promoting adhesions.
  • High PAI-2 concentrations are found in inflamed peritoneal tissue, but not in normal tissue.
  • The cellular source of PAI-2 in the peritoneum during inflammation was previously unknown.

Purpose of the Study:

  • To localize the production of plasminogen activator inhibitor-2 (PAI-2) within peritoneal tissue using in situ mRNA hybridization.
  • To identify the specific cell types responsible for PAI-2 gene expression in normal and inflamed appendix.

Main Methods:

  • In situ mRNA hybridization using a digoxigenin-labeled cDNA probe on normal and inflamed human appendix sections.
  • Immunohistochemistry was used to confirm cell identities with cell-specific markers.

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  • Control experiments included incubation with plasmid DNA or ribonuclease-digested PAI-2 probe.

    • Main Results:

    • In normal appendix, PAI-2 mRNA was localized to macrophages in the mucosa.
    • In inflamed appendix, PAI-2 mRNA was found in macrophages with wider distribution and also in mesothelial cells.
    • PAI-2 expression was specific to inflamed mesothelial cells, not present in normal mesothelial cells.

    Conclusions:

    • Macrophages are a source of PAI-2 in normal peritoneum.
    • Mesothelial cells in inflamed peritoneum also produce PAI-2, contributing to fibrin deposition.
    • Identifying PAI-2 producing cells enhances understanding of peritonitis pathophysiology and adhesion formation.