Troubleshooting in platelet storage temperature and new perspectives through proteomics.

Abstract

Platelets represent a key cellular blood component under physiological conditions, due to their implications in the maintenance of vascular integrity and prevention of haemorrhagic phenomena1. Dysfunctions associated with thrombocytopenia constitute a significant threat to patients’ health. So far, administration of platelet concentrates (PCs) from healthy donors is the only known strategy for medical care of patients with active bleeding, thrombocytopenia caused by bone marrow dysfunctions or due to chemotherapy for treatments of malignancies, or upon preliminary treatments prior to stem cell transplantation. Qualitative and quantitative changes in platelets could also occur following coronary artery bypass surgery and trauma, and may represent a key indicator of likely thrombotic complications2. Platelets are basically collected from donors in two ways: extraction from whole blood throughout centrifugation (buffy-coat) or through apheresis. Both methods are currently employed and have bright sides and disadvantages. Analogously to other blood components, techniques to improve the shelf life of platelets (currently, only five days), while maintaining their safety and effectiveness, are under constant investigation worldwide. Indeed, blood transfusion services are always in shortage of PCs, because of the impossibility to prolong their storage in like fashion to hypothermic storage of erythrocyte concentrates or frozen storage of fresh frozen plasma. In order to improve storage of PCs, lowering temperature has been attempted as well, although results were not as positive as expected, since platelets do not tolerate refrigeration. Hypothermic (4°C) storage conditions cause deep modifications in platelet shape and functionality. These are relevant issues which compromise viability of cold stored platelets, as they exert their physiological role through their ability to change shape and activate under various conditions. Low temperature appears to be a triggering factor for activation as well, thus yielding yet activated platelets as unviable blood product at the end of the storage. This review focuses on platelet storage temperatures and the main issues which affect both current (22 °C) and alternative (4 °C) storage protocols for PCs. In particular, we herein discuss the initial events which trigger morphological and physiological changes upon cold activation, partially distinguishable from physiological activation. Moreover, a glance will be given at recent proteomic approaches, which promise to improve current knowledge on blood components of transfusion interest, mainly addressing current technical hurdles (such as the analysis of membrane proteins and their reciprocal interaction).