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Fig. 6 | Stem Cell Research & Therapy

Fig. 6

From: PINK1 contained in huMSC-derived exosomes prevents cardiomyocyte mitochondrial calcium overload in sepsis via recovery of mitochondrial Ca2+ efflux

Fig. 6

PINK1 transferred from huMSC-exo regulated mCa2+ efflux by affecting PKA activity in cardiomyocytes. a AC16 cells were treated with LPS and huMSC-exo, and FSK or FSK and H89 were added. The mCa2+ efflux of cells was detected; Ru360: MCU inhibitor, CGP: NCLX inhibitor. b Average mCa2+ efflux rates of Fig. 6a, n = 3 replicates per group; *p < 0.05, **p < 0.01. c AC16 cells were treated with LPS and Pink1-inhibited huMSC-exo, after which FSK or FSK and H89 were added. The mCa2+ efflux of cells was assessed; Ru360: MCU inhibitor, CGP: NCLX inhibitor. d Average mCa2+ efflux rates of Fig. 6c, n = 3 replicates per group; *p < 0.05. eg Mitochondrial membrane potential analysis was measured using a fluorescence probe JC-1 assay system. The images were captured using confocal microscopy, Red: mitochondrial J–aggregates, green: mitochondrial monomers (e), and the ratio of red/green fluorescence represented the level of Δψm (f, g). A high ratio indicates a high mitochondrial membrane potential; *p < 0.05, **p < 0.01

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