Fibronectin degradation: An in‐vitro model of neutrophil mediated endothelial cell damage

Kevin D. Forsyth, Roland J. Levinsky

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

We have observed that fibronectin has a characteristic fibrillar morphology within the extracellular matrix surrounding endothelial cells. This morphology, which is easily recognizable by conventional immunoperoxidase techniques, is disrupted if neutrophils are induced to degranulate on endothelial monolayers. Loss of the fibrillar morphology (degraded fibronectin) is characterized by fragmentation and diffuse spreading of fibronectin over the surface of the endothelial cells. Loss of the normal fibronectin architecture following neutrophil degranulation is more rapid and extensive in endothelium pretreated with Interleukin‐1 (IL‐1). In addition, there is loss from the fibronectin molecule of a chymotryptic protease‐sensitive epitope recognized by a cellular fibronectin specific antibody. Degraded fibronectin is stimulatory for neutrophils, and is likely to induce further fibronectin breakdown. This sequence has the potential to set up an amplification inflammatory loop with neutrophil mediated loss of vascular homeostasis. Alteration of fibronectin architecture is a useful marker of endothelial injury, and has important pathophysiological consequences.

Original languageEnglish
Pages (from-to)313-319
Number of pages7
JournalThe Journal of Pathology
Volume161
Issue number4
DOIs
Publication statusPublished - Aug 1990
Externally publishedYes

Keywords

  • adhesion
  • endothelium
  • Fibronectin
  • injury
  • Interleukin‐1
  • neutrophil

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