BACKGROUND: To reduce the risk of transfusion transmission infection, nucleic acid targeted methods have been developed to inactivate pathogens in PCs. miRNAs have been shown to play an important role in platelet function, and changes in the abundance of specific miRNAs during storage have been observed, as have perturbation effects related to pathogen inactivation (PI) methods. The aim of this work was to investigate the effects of PI on selected miRNAs during storage.STUDY DESIGN AND METHODS: Using a pool and split strategy, 3 identical buffy coat PC units were generated from a pool of 24 whole blood donors. Each unit received a different treatment: 1) Untreated platelet control in platelet additive solution (C-PAS); 2) Amotosalen-UVA-treated platelets in PAS (PI-PAS); and 3) untreated platelets in donor plasma (U-PL). PCs were stored for 7 days under standard blood banking conditions. Standard platelet quality control (QC) parameters and 25 selected miRNAs were analyzed.RESULTS: During the 7-day storage period, differences were found in several QC parameters relating to PI treatment and storage in plasma, but overall the three treatments were comparable. Out of 25 miRNA tested changes in regulation of 5 miRNA in PI-PAS and 3 miRNA U-PL where detected compared to C-PAS. A statistically significant difference was observed in down regulations miR-96-5p on Days 2 and 4, 61.9% and 61.8%, respectively, in the PI-PAS treatment. CONCLUSION:Amotosalen-UVA treatment does not significantly alter the miRNA profile of platelet concentrates generated and stored using standard blood banking conditions. P latelets play a central role in hemostasis and represent an integral part of transfusion medicine. Platelet concentrates (PCs) are normally stored at room temperature for a maximum of 5 to 7 days, depending on country-specific regulations. 1,2 One of two main reasons for this limited storage time is the potential for bacterial growth during storage. 3,4 The risk of transfusion-transmitted bacterial infections (TTBIs) due to contaminated PCs is persistent despite improved donor selection protocols, phlebotomy techniques, and PC bacterial screening. Life threatening septic transfusion reactions (STRs) related to platelet transfusions still occur. 4,5 The currently available bacterial detection assays are not sufficient to prevent TTBI. 6 The rate of STRs due to PC transfusion has likely been underestimated, as highlighted in a recent 7-year retrospective study of PC transfusions using passive and active surveillance. 7 The second reason for the relatively short shelf life of stored platelets is platelet storage lesion (PSL). PSL is a collective term for a variety of factors that describe the deterioration of platelet quality during storage. 8,9 The onset and acceleration of PSL during storage is likely to affect platelet post transfusion recovery and survival. 10,11 The onset and accumulation of PSL is related to the activation of or damage to the platelets as result of their preparation or storage conditions, and can eventual...
BACKGROUND: The risk of bacterial contamination and the deterioration of platelet (PLT) quality limit the shelf-life of platelet concentrates (PCs). The INTERCEPT pathogen inactivation system reduces the risk of pathogen transmission by inhibiting nucleic acid replication using a combination of a photo-reactive compound and UVA illumination. The goal of this study was to investigate the effects the INTERCEPT system has on the PLT metabolome and metabolic activity.From the
Platelet granules contain a diverse group of proteins. Upon activation and during storage, platelets release a number of proteins into the circulation or supernatant of stored platelet concentrate (PC). The aim of this work was to investigate the effect of pathogen inactivation (PI) on a selection of proteins released in stored platelets. Materials and Methods: PCs in platelet additive solution (PAS) were produced from whole blood donations using the buffy coat (BC) method. PCs in the treatment arm were pathogen inactivated with amotosalen and UVA, while PCs in the second arm were used as an untreated platelet control. Concentrations of 36 proteins were monitored in the PCs during storage. Results: The majority of proteins increased in concentration over the storage period. In addition, 10 of the 29 proteins that showed change had significantly different concentrations between the PI treatment and the control at one or more timepoints. A subset of six proteins displayed a PI-related drop in concentration. Conclusions: PI has limited effect on protein concentration stored PC supernatant. The protein’s changes related to PI treatment with elevated concentration implicate accelerated Platelet storage lesion (PSL); in contrast, there are potential novel benefits to PI related decrease in protein concentration that need further investigation.
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