Premium
Fibronectin degradation; An in ‐ vitro model of neutrophil mediated endothelial cell damage
Author(s) -
Forsyth Kevin D.,
Levinsky Roland J.
Publication year - 1990
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711610407
Subject(s) - fibronectin , microbiology and biotechnology , extracellular matrix , endothelium , endothelial stem cell , degranulation , chemistry , biology , in vitro , biochemistry , receptor , endocrinology
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.