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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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Atherosclerosis III: Management01:26

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In the presence of oxidizing agents, phenols are oxidized to quinones. Quinones can be easily reduced back to phenols using mild reducing agents. The electron-donating hydroxyl group enhances the reactivity of the aromatic ring, enabling oxidation of the ring even in the absence of an α hydrogen.
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Updated: Mar 21, 2026

Author Spotlight: Innovative Techniques for ROS Detection and Implications for Platelet Research
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Mildly oxidized HDL decrease agonist-induced platelet aggregation and release of pro-coagulant platelet extracellular

M Tafelmeier1, A Fischer1, E Orsó1

  • 1Institute for Clinical Chemistry and Laboratory Medicine, University Clinic of Regensburg Franz-Josef-Strauss-Allee 11, D-93052 Regensburg, Germany.

The Journal of Steroid Biochemistry and Molecular Biology
|May 11, 2016
PubMed
Summary
This summary is machine-generated.

Mildly oxidized HDL (moxHDL) can improve platelet concentrate (PLC) quality by reducing platelet extracellular vesicle (PL-EV) release and enhancing platelet lipid homeostasis, potentially prolonging storage viability.

Keywords:
AggregationExtracellular vesicleMildly oxidized HDLPlatelet concentrateStorage lesion

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Area of Science:

  • Biochemistry
  • Hematology
  • Lipidomics

Background:

  • Stored platelet concentrates (PLCs) develop platelet storage lesion (PSL), impairing platelet (PLT) viability and function.
  • Oxidized high-density lipoprotein (oxHDL) effects on PLTs are poorly understood, unlike oxidized low-density lipoprotein (oxLDL).

Purpose of the Study:

  • To investigate the impact of native HDL (nHDL) and mildly oxidized HDL (moxHDL) on PLCs during storage.
  • To analyze the effects of moxHDL on platelet extracellular vesicle (PL-EV) release, aggregation, and lipid profiles.

Main Methods:

  • PLCs were treated with nHDL or moxHDL under blood banking conditions for 5 days.
  • Analyses included flow cytometry, nanoparticle tracking analysis (NTA), aggregometry, immunoblotting, and mass spectrometry.
  • Evaluated PL-EV release, PLT aggregation, protein expression, and lipid composition.

Main Results:

  • MoxHDL significantly decreased PL-EV release by 36% and partially reversed agonist-induced PLT aggregation compared to nHDL.
  • MoxHDL improved PLT membrane lipid homeostasis via enhanced lysophospholipid uptake and remodeling, increasing the sphingomyelin/ceramide ratio.
  • CD36 and scavenger receptor-B1 (SR-B1) protein content increased in secreted PL-EVs.

Conclusions:

  • MoxHDL improves PLT membrane lipid homeostasis and antagonizes PL-EV release and aggregation in stored PLCs.
  • This effect is likely due to enhanced lipid remodeling mediated by CD36 and SR-B1.
  • MoxHDL shows potential as an in vitro supplement to improve PLC quality and extend storage duration.