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High-density lipoprotein 3 and apolipoprotein A-I alleviate platelet storage lesion and release of platelet

Annika Pienimaeki-Roemer1, Astrid Fischer, Maria Tafelmeier

  • 1Institute for Clinical Chemistry and Laboratory Medicine, Regensburg, Germany.

Transfusion
|June 11, 2014
PubMed

Insights

High-density lipoprotein 3 (HDL3) and apolipoprotein A-I (apoA-I) improve platelet storage by reducing extracellular vesicle release and enhancing lipid homeostasis. These agents can improve platelet concentrate quality for longer storage.

Area of Science:

  • Biochemistry
  • Hematology
  • Lipidomics

Background:

  • Stored platelet concentrates (PLCs) develop a storage lesion (PSL), reducing viability and function.
  • Platelet extracellular vesicle (PL-EV) release and lipidomic changes are key features of PSL.
  • High-density lipoprotein 3 (HDL3) is known to improve platelet homeostasis.

Purpose of the Study:

  • To investigate HDL3 and apolipoprotein A-I (apoA-I) as agents to counteract the platelet storage lesion (PSL).
  • To assess the effects of HDL3 and apoA-I on PLT viability, function, and lipid profiles during storage.

Main Methods:

  • Healthy donor PLCs were incubated with native HDL3 (nHDL3) or apoA-I for 5 days.
  • Analyses included flow cytometry, Born aggregometry, and lipid mass spectrometry.
  • Evaluated PL-EV release, PLT aggregation, surface marker expression, and lipid compositions.

Main Results:

  • nHDL3 and apoA-I significantly reduced PL-EV release by up to 62%.
  • These agents counteracted PLT lipid loss and altered cholesteryl ester (CE)/free cholesterol (FC) ratios.
  • nHDL3 administration improved PLT bis(monoacylglycero)phosphate/phosphatidylglycerol and phosphatidic acid/lysophosphatidic acid ratios, enhancing PLT aggregation.

Conclusions:

  • nHDL3 and apoA-I improve PLT membrane homeostasis, intracellular lipid processing, and CE efflux, antagonizing PSL.
  • These findings suggest potential for nHDL3 or apoA-I as supplements to improve PLC quality and storage duration.
  • Uptake of nHDL3 into the PLT open canalicular system is proposed.
Abstract

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