Pienimaeki-Roemer, Annika and Fischer, Astrid and Tafelmeier, Maria and Orso, Evelyn and Konovalova, Tatiana and Boettcher, Alfred and Liebisch, Gerhard and Reidel, Armin and Schmitz, Gerd (2014) High-density lipoprotein 3 and apolipoprotein A-I alleviate platelet storage lesion and release of platelet extracellular vesicles. TRANSFUSION, 54 (9). pp. 2301-2314. ISSN 0041-1132, 1537-2995
Full text not available from this repository. (Request a copy)Abstract
BackgroundStored platelet (PLT) concentrates (PLCs) for transfusion develop a PLT storage lesion (PSL), decreasing PLT viability and function with profound lipidomic changes and PLT extracellular vesicle (PL-EV) release. High-density lipoprotein 3 (HDL3) improves PLT homeostasis through silencing effects on PLT activation in vivo. This prompted us to investigate HDL3 and apolipoprotein A-I (apoA-I) as PSL-antagonizing agents. Study Design and MethodsHealthy donor PLCs were split into low-volume standard PLC storage bags and incubated with native (n)HDL3 or apoA-I from plasma ethanol fractionation (precipitate IV) for 5 days under standard blood banking conditions. Flow cytometry, Born aggregometry, and lipid mass spectrometry were carried out to analyze PL-EV release, PLT aggregation, agonist-induced PLT surface marker expression, and PLT and plasma lipid compositions. ResultsCompared to control, added nHDL(3) and apoA-I significantly reduced PL-EV release by up to -62% during 5 days, correlating with the added apoA-I concentration. At the lipid level, nHDL(3) and apoA-I antagonized PLT lipid loss (+12%) and decreased cholesteryl ester (CE)/free cholesterol (FC) ratios (-69%), whereas in plasma polyunsaturated/saturated CE ratios increased (+3%) and CE 16:0/20:4 ratios decreased (-5%). Administration of nHDL(3) increased PLT bis(monoacylglycero)phosphate/phosphatidylglycerol (+102%) and phosphatidic acid/lysophosphatidic acid (+255%) ratios and improved thrombin receptor-activating peptide 6-induced PLT aggregation (+5%). ConclusionnHDL(3) and apoA-I improve PLT membrane homeostasis and intracellular lipid processing and increase CE efflux, antagonizing PSL-related reduction in PLT viability and function and PL-EV release. We suggest uptake and catabolism of nHDL(3) into the PLT open canalicular system. As supplement in PLCs, nHDL(3) or apoA-I from Fraction IV of plasma ethanol fractionation have the potential to improve PLC quality to prolong storage.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TANDEM MASS-SPECTROMETRY; LECITHIN-CHOLESTEROL ACYLTRANSFERASE; HIGH-THROUGHPUT QUANTIFICATION; HUMAN-BLOOD PLATELETS; FOAM CELL-FORMATION; LYSOPHOSPHATIDIC ACID; SCAVENGER RECEPTOR; ESI-MS/MS; SR-BI; MICROPARTICLES; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 27 Aug 2019 13:12 |
| Last Modified: | 27 Aug 2019 13:12 |
| URI: | https://pred.uni-regensburg.de/id/eprint/9643 |
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