Scientific article

E-selectin binding promotes neutrophil activation in vivo in E-selectin transgenic mice

Published inBiochemical and biophysical research communications, vol. 224, no. 3, p. 825-830
Publication date1996

E-selectin is a membrane protein expressed by endothelial cells activated by cytokines released during the inflammatory process; it plays an important role in neutrophil emigration into inflamed tissues. To further explore in vivo the function of E-selectin, we have generated transgenic mouse line expressing E-selectin under the control of a chicken beta-actin promoter. In these mice, the number of blood neutrophils was reduced, without any other obvious phenotype or tissue damage. These neutrophils, however, displayed two significant changes: first, an alteration in the levels of expression of two membrane receptors involved in neutrophil adhesion to endothelial cells, namely a marked increased in the Mac-1 antigen (CD11b/CD18) and a decrease in the Mel-14 antigen (L-selectin); second, an increased oxidative activity when compared to blood neutrophils of non-transgenic mice, as shown by their capacity to oxidize 2',7'-dichlorofluorescein (DCFH) into a fluorescent compound. These observations indicate that the binding of E-selection with neutrophils bearing its ligands promotes neutrophil activation in vivo.

  • Actins/genetics
  • Animals
  • Base Sequence
  • Bone Marrow/metabolism
  • Bone Marrow Cells
  • E-Selectin/genetics/ metabolism
  • Fluorescence
  • Liver/metabolism
  • Lymphocyte Activation
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Muscles/metabolism
  • Myocardium/metabolism
  • Neutrophil Activation
  • Neutrophils/ immunology/metabolism
  • Promoter Regions, Genetic
  • Protein Binding
  • RNA, Messenger/genetics
Citation (ISO format)
ARAKI, Masatake et al. E-selectin binding promotes neutrophil activation in vivo in E-selectin transgenic mice. In: Biochemical and biophysical research communications, 1996, vol. 224, n° 3, p. 825–830.
Main files (1)
ISSN of the journal0006-291X

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