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Related Experiment Videos

Modulation of endotoxin-induced endothelial activity by microtubule depolymerization.

Joseph Cuschieri1, David Gourlay, Iris Garcia

  • 1Department of Surgery, Division of Trauma/Critical Care, University of Cincinnati, 231 Albert Sabin Way, ML 558, Cincinnati, OH 45267-0558, USA. cush98@aol.com

The Journal of Trauma
|January 25, 2003
PubMed
Summary

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Microtubule polymerization is crucial for endotoxin-induced signaling, leading to neutrophil adhesion. Disrupting microtubules significantly reduces this adhesion, offering potential therapeutic benefits in sepsis.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Signaling

Background:

  • Endotoxin triggers Toll-mediated pathways and microtubule polymerization in endothelial cells, potentially influencing neutrophil migration.
  • The precise role of endotoxin-induced microtubule polymerization in cellular signaling remains unclear.

Purpose of the Study:

  • To investigate the role of microtubule polymerization in endotoxin-induced endothelial cell signaling and neutrophil adhesion.
  • To determine if inhibiting microtubule polymerization affects Toll-mediated pathways and subsequent inflammatory responses.

Main Methods:

  • Human umbilical vein endothelial cells were treated with endotoxin and colchicine (a microtubule depolymerizing agent).
  • Toll-mediated signaling, protein production (Western blot, gel shift, ELISA), and neutrophil adhesion (fluorometry) were analyzed.

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Main Results:

  • Endotoxin activated Toll pathways, increasing intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) production, promoting neutrophil adhesion.
  • Colchicine selectively modulated signaling pathways, inhibiting some (ERK1/2, JNK) while enhancing others (p38).
  • Microtubule disruption attenuated ICAM-1, IL-8, and prostaglandin E2 production, reduced cyclooxygenase-2 expression, and significantly decreased neutrophil adhesion.

Conclusions:

  • Microtubule formation is essential for optimal endotoxin-induced signaling via specific pathways (ERK1/2, JNK, AP-1).
  • Inhibition of microtubule polymerization reduces the proadhesive phenotype of endothelial cells.
  • This suggests that targeting microtubule dynamics could be a strategy to modulate neutrophil recruitment in sepsis.