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Mechano-Redox Control of Mac-1 De-Adhesion by PDI Promotes Directional Movement Under Flow.

Alexander Dupuy1,2, Camilo Aponte-Santamaría3, Adva Yeheskel4

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|April 6, 2023
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Summary

Protein disulfide isomerase (PDI) cleaves a specific disulfide bond in Mac-1 (CD11b/CD18), enabling neutrophil migration during inflammation. This molecular mechanism controls Mac-1

Keywords:
cell movementdisulfidesintegrinsmicrofluidicsneutrophilsshear strength

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Neutrophil migration is crucial for inflammation initiation and resolution.
  • Macrophage-1 antigen (Mac-1) is essential for neutrophil adhesion and migration under shear forces.
  • Protein disulfide isomerase (PDI) influences neutrophil adhesion and migration.

Purpose of the Study:

  • To elucidate the molecular mechanism of PDI control over Mac-1 affinity for ICAM-1 during neutrophil migration under fluid shear.
  • To investigate how PDI regulates Mac-1 function in neutrophil motility.

Main Methods:

  • Neutrophil perfusion over ICAM-1 coated microfluidic chips.
  • Confocal microscopy to visualize Mac-1 and PDI colocalization.
  • Mass spectrometry to map Mac-1 disulfide bond redox states.
  • Recombinant Mac-1 expression and ligand affinity measurements.
  • Molecular dynamics simulations and conformation-specific antibodies to study Mac-1 conformations.
  • Assessment of neutrophil crawling on ICAM-1 and inflamed endothelial cells with PDI inhibition.

Main Results:

  • PDI colocalized with high-affinity Mac-1 at the trailing edge of crawling neutrophils.
  • PDI cleaved specific disulfide bonds (C169-C176 and C224-C264) in the Mac-1 βI domain.
  • Cleavage of the C224-C264 bond selectively controlled Mac-1 disengagement from ICAM-1 under shear.
  • This cleavage induced conformational changes and mechanical stress, reducing Mac-1 affinity and promoting directional migration.
  • PDI inhibition reduced neutrophil migration on inflamed endothelial cells.

Conclusions:

  • Shear-dependent PDI cleavage of the Mac-1 C224-C264 disulfide bond triggers Mac-1 de-adherence from ICAM-1.
  • This process enables directional neutrophil movement during inflammation.
  • PDI plays a key role in regulating neutrophil motility under flow conditions.