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Platelet inhibition by hypochlorous acid involves cAMP signalling.

Lorna O'Donoghue1, Dishon Hiebner2, Roopesh Krishnankutty3

  • 1UCD School of Medicine, UCD Conway Institute, University College Dublin, Dublin 4, Belfield, Ireland; Irish Centre for Vascular Biology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin D02 YN77, Ireland.

Cellular Signalling
|December 17, 2024
PubMed
Summary

Hypochlorous acid (HOCl) inhibits platelet aggregation and spreading by oxidizing cysteine residues in key proteins. This mechanism involves the cAMP pathway and regulation of Rap1, revealing neutrophil-platelet crosstalk.

Keywords:
AggregationHypochlorous acidNeutrophilsPlateletscAMP

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Area of Science:

  • Biochemistry
  • Hematology
  • Immunology

Background:

  • Neutrophil-derived hypochlorous acid (HOCl) is implicated in platelet inhibition.
  • The precise molecular mechanisms underlying HOCl's effects on platelets remain largely undescribed.

Purpose of the Study:

  • To elucidate the mechanisms by which HOCl affects platelet function.
  • To identify specific proteins and pathways modulated by HOCl in platelets.

Main Methods:

  • Platelet morphology, spreading, and aggregation assays following HOCl exposure.
  • Mass spectrometry-based proteomics to identify oxidized proteins.
  • Measurement of cAMP levels and VASP phosphorylation.
  • Assessment of Rap1 activation.

Main Results:

  • HOCl exposure altered platelet morphology and inhibited spreading and aggregation, effects reversible by glutathione.
  • Proteomic analysis identified oxidized cysteine residues in 37 proteins, including adenylate cyclase 6 and Rap1B.
  • HOCl stimulated cAMP production and VASP phosphorylation, while inhibiting Rap1-GTP formation.

Conclusions:

  • HOCl inhibits platelet function, at least partly, via the cAMP pathway and regulation of Rap1.
  • This study reveals novel insights into HOCl-mediated crosstalk between neutrophils and platelets.