Role of Accessory Molecule(s) in Endotoxin-Endothelial Interactions and Endothelial Barrier Dysfunction.

Abstract

We have studied the direct impact of endotoxin or bacterial lipopolysaccharide (LPS) on pulmonary vascular endothelial cell (EC) barrier function. We have found that LPS induces (1) tyrosine phosphorylation of a 65kDa protein, paxillin, (2) actin disassembly, and (3) opening of the paracellular pathway. The tyrosine phosphorylation events were clearly prerequisite to the downstream events of actin depolymerization, opening of the paracellular pathway, and loss of endothelial barrier function.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 1997
Accession Number
ADA331555

Entities

People

  • Simeon E. Goldblum

Organizations

  • University of Maryland School of Medicine

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Anti-Bacterial Agents
  • Arteries
  • Biological Sciences
  • Blood Coagulation Factors
  • Cell Membrane Structures
  • Cells
  • Chemistry
  • Cytoskeleton
  • Dysfunction
  • Endothelial Cells
  • Escherichia Coli
  • Genetic Structures
  • Laboratory Animals
  • Materials
  • Molecules
  • Proteins

Fields of Study

  • Biology

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