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The adhesion receptor CD-31 can be primed to rapidly adjust the neutrophil cytoskeleton.

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Author

Summary, in English

The adhesion receptor CD-31 is expressed on neutrophils and endothelial cells and participates in transendothelial migration of neutrophils. Although necessary, information on CD-31-induced signaling and its influence on the shape-forming actin network is scarce. Here, we found that antibody engagement of CD-31 on suspended neutrophils triggered a prompt intracellular Ca(2+) signal, providing the cells had been primed with a chemotactic factor. Inhibition of Src-tyrosine kinases blocked this Ca(2+) signal, but not a fMet-Leu-Phe-induced Ca(2+) signal. Despite the ability of fMet-Leu-Phe to activate Src-tyrosine kinases, it did not per se induce tyrosine phosphorylation of CD-31. However, fMet-Leu-Phe did enable such a phosphorylation following an antibody-induced engagement of CD-31. This clustering also triggered a Ca(2+)-dependent depolymerization of actin and, surprisingly enough, a simultaneous polymerization. The ability of CD-31 to signal dynamic alterations in the cytoskeleton, particularly the Ca(2+)-induced actin depolymerization, further explains how neutrophils can squeeze themselves out between adjacent endothelial cells.

Publishing year

2002

Language

English

Pages

1092-1097

Publication/Series

Biochemical and Biophysical Research Communications

Volume

292

Issue

4

Document type

Journal article

Publisher

Elsevier

Topic

  • Biological Sciences

Keywords

  • CD31 : drug effects
  • Antigens
  • Antibodies : pharmacology
  • Actins : metabolism
  • Cytoskeleton : metabolism
  • Enzyme Inhibitors : pharmacology
  • Human
  • Intracellular Fluid : metabolism
  • N-Formylmethionine Leucyl-Phenylalanine : pharmacology
  • Neutrophils : cytology
  • Neutrophils : metabolism
  • Phosphorylation : drug effects
  • Signal Transduction : drug effects
  • Signal Transduction : physiology
  • Support
  • Non-U.S. Gov't
  • src-Family Kinases : antagonists & inhibitors
  • CD31 : metabolism
  • Calcium : metabolism
  • Calcium Signaling : drug effects
  • Cell Adhesion : physiology
  • Cell Movement : physiology
  • Chemotactic Factors : pharmacology

Status

Published

Research group

  • Experimental Pathology, Malmö

ISBN/ISSN/Other

  • ISSN: 1090-2104