Calcium flux in neutrophils synchronizes β2 integrin adhesive and signaling events that guide inflammatory recruitment

Ulrich Y. Schaff, Itsukyo Yamayoshi, Tiffany Tse, Donald Griffin, Lilian Kibathi, Scott I. Simon

Research output: Contribution to journalArticle

55 Scopus citations

Abstract

Intracellular calcium flux is an early step in the signaling cascade that bridges ligation of selectin and chemokine receptors to activation of adhesive and motile functions during recruitment on inflamed endothelium. Calcium flux was imaged in real time and provided a means of correlating signaling events in neutrophils rolling on E-selectin and stimulated by chemokine in a microfluidic chamber. Integrin dependent neutrophil arrest was triggered by E-selectin tethering and ligation of IL-8 seconds before a rapid rise in intracellular calcium, which was followed by the onset of pseudopod formation. Calcium flux on rolling neutrophils increased in a shear dependent manner, and served to link integrin adhesion and signaling of cytoskeletally driven cell polarization. Abolishing calcium influx through membrane expressed store operated calcium channels inhibited activation of high affinity β2 integrin and subsequent cell arrest. We conclude that calcium influx at the plasma membrane integrates chemotactic and adhesive signals, and functions to synchronize signaling of neutrophil arrest and migration in a shear stress dependent manner.

Original languageEnglish (US)
Pages (from-to)632-646
Number of pages15
JournalAnnals of Biomedical Engineering
Volume36
Issue number4
DOIs
StatePublished - Apr 2008

Keywords

  • Calcium signaling
  • Integrin affinity
  • Neutrophils
  • Shear stress

ASJC Scopus subject areas

  • Biomedical Engineering

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