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Related Experiment Videos

Signal transduction pathway in endothelial dysfunction.

Chumpon Wilasrusmee1, Gaurang Shah, Smita Kittur

  • 1Department of Surgery, SUNY Upstate Medical University, Syracuse, New York 13210, USA.

Surgical Infections
|May 15, 2004
PubMed
Summary

Protein tyrosine phosphatase and protein kinase C inhibition cause endothelial dysfunction by disrupting capillary networks. These findings are crucial for understanding sepsis and infectious conditions.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pathophysiology

Background:

  • Endothelial dysfunction is a key feature of sepsis and ARDS.
  • An in vitro model using basement membrane matrix (Matrigel) was previously established to study endothelial dysfunction.
  • This study investigates signal transduction pathways leading to endothelial cell dysfunction and capillary disruption in infectious conditions.

Purpose of the Study:

  • To define signal transduction pathways involved in endothelial dysfunction.
  • To elucidate mechanisms of capillary disruption in sepsis and infectious diseases.
  • To identify key enzymes regulating endothelial cell function in vitro.

Main Methods:

  • Human aortic endothelial cells (HAEC) were cultured on a laminin-rich matrix to form capillary networks.

Related Experiment Videos

  • HAECs were treated with inhibitors of protein tyrosine phosphatase (sodium orthovanadate), phosphoinositon-3-phosphate (wortmannin), or protein kinase C (bisindolylmaleimide).
  • Capillary tube formation was quantified by counting network intersections; statistical significance was determined by ANOVA.

    • Main Results:

    • Inhibition of protein tyrosine phosphatase and protein kinase C led to significant endothelial dysfunction and reduced capillary networks.
    • Sodium orthovanadate and bisindolylmaleimide significantly decreased capillary network formation and disrupted mature tubes at higher concentrations.
    • Inhibition of phosphoinositon-3-phosphate did not cause endothelial dysfunction.

    Conclusions:

    • Protein kinase C and protein tyrosine phosphatase play critical roles in endothelial dysfunction.
    • Interference with phosphorylation signals within endothelial cells contributes to dysfunction.
    • These pathways are potentially significant in the pathophysiology of sepsis and other infections.