Stored platelet concentrates produced by the platelet‐rich plasma method are more resistant to apoptosis but more sensitive to activation than are platelets prepared by the buffy‐coat and apheresis methods

Recently, we studied the contributions of PLT activation and apoptosis to the PLT storage lesion during conventional (Days 2-5), extended (Days 6-8), and long-term (Days 11-16) storage of leukoreduced PCs produced by the PLT-rich plasma method (PRP-PCs). Four apoptotic parameters, including depolarization of mitochondrial inner membrane potential (DYm), caspase-3 activation, phosphatidylserine (PS) exposure, and release of PLT microparticles, were used for quantifying mitochondrial, cytoplasmic, plasma membrane, and cellular manifestations of PLT apoptosis, respectively, and PLT activation was determined by P-selectin (CD62) exposure. It was demonstrated that PLT activation and apoptosis responses are triggered sequentially, rather than in parallel, during storage of PRP-PCs. PLT activation was readily induced under the conventional and extended PLT storage, whereas triggering of PLT apoptosis required long-term storage. Furthermore, for all storage days, the level of PLT activation reached was significantly higher than the level of apoptosis. Different results have been reported in the subsequent publication of Albanyan and coworkers, in which PLT activation and apoptosis phenomena during storage for 1, 3, 5, and 7 days were studied in leukoreduced PCs produced by the buffy coat (BC-PCs) and apheresis (APPCs) methods. The aim of the current report is to compare PLT activation and apoptosis responses in PRP-PCs versus BC-PCs and AP-PCs by analyzing results of these closely related studies. Table 1 summarizes the reported data on the dynamics of DYm depolarization and caspase-3 activation in PRP-, BC-, and AP-PCs. In PRP-PCs, DYm depolarization and caspase-3 activation did not increase significantly even after long-term storage for up to 12 days; storage for 13-14 days was required for significant triggering of these apoptotic events. In contrast, much faster apoptotic changes were observed during storage of BC-PCs and AP-PCs: when DYm depolarization was measured by the red-to-green fluorescence ratio of the DYmdetecting dye JC-1, as was employed in our study, DYm depolarization was significantly increased by Days 5 and 7 (Table 1). However, when DYm depolarization was measured by an alternative JC-1 method, as the percentage of PLTs with depolarized DYm, which detects cells with full DYm depolarization, only BC-PCs, but not AP-PCs, showed this apoptotic alteration on Days 5 and 7 (Fig. 1B, right panel in Albanyan et al.). As evidenced from the data on the sequential dynamics (Table 1) and the magnitude of PLT apoptosis and activation responses, as measured by PS and CD62 exposure, respectively (Table 2), the ability of PLT apoptosis and activation to be induced by PLT storage differs significantly in PRP-PCs, in comparison to BC-PCs and AP-PCs. In PRP-PCs, PLT apoptosis is more resistant to PLT storage than PLT activation (Table 2, Column 2, p < 0.001 for Days 2, 5, and 7); in contrast, in BC-PCs and AP-PCs, PLT apoptosis and activation have approximately equal sensitivity to storage (Table 2, Columns 3 and 4, 18.6%-21.3% vs. 20%-25% for Day 7). Furthermore, PLT apoptosis in PRPPCs is more resistant to storage than is apoptosis in BC-PCs and AP-PCs (Tables 1 and 2A, Columns 2-4, p < 0.01 for Days 5 and 7); in contrast, activation in PRPPCs is more sensitive to storage than is activation in BC-PCs and AP-PCs (Table 2B, Columns 2-4, 65.8 9.7% vs. 20%-25% for Day 7). In conclusion, the analysis of these recently reported data indicates that PLT activation rather than apoptosis most contributes to the PLT storage lesion during storage of PRP-PCs for 7 days. Therefore, PLT activation, and not apoptosis, should be the main concern in maintaining quality of PRP-PCs during blood banking storage. In contrast, for BC-PCs and AP-PCs, both activation and