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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 

Endothelin-1 induces production of the neutrophil chemotactic factor interleukin-8 by human brain-derived endothelial cells.

Increased levels of endothelin-1 ( Et-1), a potent vasoconstrictor, have been correlated with hypertension and neuronal damage in ischemic/ reperfusion injury. The presence of polymorphonuclear cells (PMNs) in the brain has been shown to be directly responsible for this observed pathology. To address the question of whether Et-1 plays a role in this process, human brain-derived endothelial cells (CNS-ECs) were cultured with Et-1. The results demonstrate that Et-1 induces production of the neutrophil chemoattractant interleukin-8 ( IL-8) twofold to threefold after 72 hours; mRNA was maximal after 1 hour of stimulation. Conditioned culture medium derived from Et-1-stimulated CNS-ECs induced a chemotactic response in the PMN migration assay. The inflammatory cytokines tumor necrosis factor-alpha ( TNF) and IL-1beta functioned additively with Et-1 in increasing IL-8 production. In contrast, transforming growth factor-beta ( TGF-beta), but not IL-10, completely abolished the effect of Et-1 on IL-8 production. However, Et-1 did not modulate intercellular adhesion molecule-1 ( ICAM-1) expression. These data demonstrate that Et-1 may be a risk factor in ischemic/ reperfusion injury by inducing increased levels of the neutrophil chemoattractant IL-8.[1]

References

  1. Endothelin-1 induces production of the neutrophil chemotactic factor interleukin-8 by human brain-derived endothelial cells. Hofman, F.M., Chen, P., Jeyaseelan, R., Incardona, F., Fisher, M., Zidovetzki, R. Blood (1998)
 
 
 
 
 
 
 
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