Irreversible oxidations of platelet proteins after riboflavin-UVB pathogen inactivation

G Sonego1, M Abonnenc2, D Crettaz2

  • 1Laboratoire de recherche sur les produits sanguins, recherche et développement produits, transfusion interrégionale CRS, Épalinges, Switzerland; Faculté de biologie et de médecine, université de Lausanne, Lausanne, Switzerland.

Insights

Pathogen inactivation treatment of platelets increases oxidative stress, impacting platelet function. Proteomics revealed specific protein oxidation changes affecting aggregation and shape post-treatment.

Area of Science:

  • Blood banking and transfusion medicine
  • Proteomics and mass spectrometry
  • Biochemistry and molecular biology

Background:

  • Pathogen inactivation technologies can alter platelet properties.
  • Reactive oxygen species generated during treatment may accelerate platelet storage lesion.
  • Proteomic studies are crucial for understanding treatment-induced protein alterations.

Purpose of the Study:

  • To investigate the impact of riboflavin/UVB pathogen inactivation on platelet proteome oxidation.
  • To identify specific oxidized proteins and their functional implications in treated platelets.

Main Methods:

  • Platelet concentrates were prepared and subjected to riboflavin/UVB pathogen inactivation.
  • Liquid chromatography-tandem mass spectrometry was used for shotgun proteomic analysis.
  • Site-specific oxidation of peptides was quantified at day 2 of storage.

Main Results:

  • Shotgun proteomics identified 2534 proteins and 9350 peptides, with 1714 oxidized.
  • Eighteen peptides were exclusively oxidized in treated platelets, while 3 were exclusively oxidized in controls.
  • Interference with proteins crucial for platelet aggregation and shape change (e.g., talin, vinculin) was observed.

Conclusions:

  • Riboflavin/UVB pathogen inactivation induces site-specific oxidation in platelet proteins.
  • Oxidative stress impacts key proteins involved in platelet aggregation and shape.
  • These findings provide insights into the mechanisms underlying altered platelet function after pathogen inactivation.

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