p38 mitogen-activated protein kinase regulates mitochondrial function and microvesicle release in riboflavin- and ultraviolet light-treated apheresis platelet concentrates

Biochemical analyses of mechanisms triggered in platelets (PLTs) upon pathogen inactivation (PI) are crucial to further understand the impact of PI on PLT functionality and, subsequently, quality.PLT concentrates (PCs) were split into four small illumination bags: 1) untreated control, 2) treated with riboflavin and ultraviolet light (RF/UV), and spiked with 3) solvent control dimethyl sulfoxide and 4) p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 before RF/UV treatment. Flow cytometry was used to monitor PLT mitochondrial potential (ΔΨRF/UV treatment triggered an increased mitochondrial translocation of both Bax and Bid (p 0.05, Day 7) and cytochrome c release (p 0.01, Day 7), loss of ΔΨThese findings further our understanding of mechanisms in PLTs initiated by the RF/UV treatment, demonstrating that this treatment induces p38 MAPK-dependent mitochondrial signaling and MV release in apheresis PCs.