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Related Experiment Videos

Neutrophil elastase enhances intercellular adhesion molecule-1 expression

Y Yamaguchi1, F Matsumura, F S Wang

  • 1Department of Surgery II, Kumamoto University Medical School, Honjo, Japan.

Transplantation
|July 17, 1998
PubMed
Summary

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Human neutrophil elastase (NE) inhibition reduces reperfusion injury by decreasing intercellular adhesion molecule-1 (ICAM-1) expression in pancreatic grafts. This study reveals NE stimulates ICAM-1 via intracellular calcium and phospholipase C signaling pathways.

Area of Science:

  • Transplantation immunology
  • Inflammatory signaling pathways
  • Vascular biology

Background:

  • Neutrophil elastase (NE) mediates inflammatory tissue damage.
  • Intercellular adhesion molecule-1 (ICAM-1) is implicated in reperfusion injury.
  • Investigating NE inhibition's effect on ICAM-1 in pancreatic transplantation.

Purpose of the Study:

  • To evaluate the efficacy of a human neutrophil elastase (NE) inhibitor (ONO-5046) in mitigating reperfusion injury.
  • To assess the impact of NE inhibition on intercellular adhesion molecule-1 (ICAM-1) expression in pancreatic grafts.
  • To elucidate the in vitro mechanisms by which NE influences ICAM-1 mRNA transcription in endothelial cells.

Main Methods:

  • In vivo study: Pancreaticoduodenal transplantation in rats with ONO-5046 administration.

Related Experiment Videos

  • ICAM-1 expression analysis using immunostaining and Northern analysis.
  • In vitro study: NE and various inhibitors tested on ICAM-1 mRNA in rat (WK-5) and human (HUVEC) endothelial cells.

    • Main Results:

    • ONO-5046 pretreatment significantly reduced ICAM-1 immunostaining and mRNA levels in transplanted pancreatic grafts.
    • NE stimulated ICAM-1 mRNA expression in WK-5 and HUVEC, an effect inhibited by ONO-5046.
    • NE-induced ICAM-1 expression was modulated by calcium ionophore, phospholipase C inhibitor, calcium chelator, and NF-κB inhibitor.

    Conclusions:

    • Human neutrophil elastase (NE) stimulates ICAM-1 expression in pancreatic grafts.
    • The mechanism involves intracellular calcium (Ca2+) influx and phospholipase C signal transduction.
    • NE inhibition represents a potential therapeutic strategy for reducing inflammatory damage in transplantation.