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Biochim Biophys Acta Mol Cell Biol Lipids. 2019 Aug;1864(8):1168-1182. doi: 10.1016/j.bbalip.2019.03.011. Epub 2019 Apr 10.

Lipid mediators in platelet concentrate and extracellular vesicles: Molecular mechanisms from membrane glycerophospholipids to bioactive molecules.

Author information

1
EV Group, Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Biocenter 1, Viikinkaari 9, 00790 Helsinki, Finland; Finnish Red Cross Blood Service, Kivihaantie 7, 00310 Helsinki, Finland.
2
Finnish Red Cross Blood Service, Kivihaantie 7, 00310 Helsinki, Finland; Helsinki University Lipidomics Unit, Helsinki Institute for Life Science (HiLIFE), Biocenter 3, Viikinkaari 1, 00790 Helsinki, Finland.
3
Lipid Mediator Unit, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, United Kingdom.
4
Finnish Red Cross Blood Service, Kivihaantie 7, 00310 Helsinki, Finland.
5
Helsinki University Lipidomics Unit, Helsinki Institute for Life Science (HiLIFE), Biocenter 3, Viikinkaari 1, 00790 Helsinki, Finland; Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland.
6
EV Group, Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki, Biocenter 1, Viikinkaari 9, 00790 Helsinki, Finland.
7
Finnish Red Cross Blood Service, Kivihaantie 7, 00310 Helsinki, Finland. Electronic address: saara.laitinen@bloodservice.fi.

Abstract

Platelets are collected for transfusion to patients with different haematological disorders, and for logistical reasons, platelets are stored as concentrates. Despite carefully controlled conditions, platelets become activated during storage, and platelet concentrates (PlaCs) may cause adverse inflammatory reactions in recipients. The time-dependent changes in the lipidome of clinical PlaCs, platelets isolated from PlaCs, and extracellular vesicles (EVs) thereof were examined by mass spectrometry. The relative amount of arachidonic acid containing glycerophospholipids, especially those in the phosphatidylethanolamine and phosphatidylserine classes during storage, but the relative amount of other polyunsaturated fatty acid containing glycerophospholipids remained stable in all sample types. These changes were not directly translated to lipid mediator (LM) profile since the levels of arachidonic acid-derived proinflammatory LMs were not specifically elevated. Instead, several monohydroxy pathway markers and functionally relevant LMs, both proinflammatory and proresolving, were detected in the PlaCs and the EVs, and some representatives of both kind clearly accumulated during storage. By Western blot, the key enzymes of these pathways were shown to be present in platelets, and in many cases, EVs. Since the EVs were enriched in the fatty acid precursors of LMs in their (phospholipid) membranes, harboured LM-producing enzymes, contained the related monohydroxy pathway markers, and secreted the final LM products, PlaC-derived EVs could participate in the regulation of inflammation and healing, and thereby aid the platelets in exerting their essential physiological functions.

KEYWORDS:

Extracellular vesicle; Glycerophospholipid; Immunology; Lipid mediator; Platelet; Specialized proresolving mediator

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