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Figure 5 | Critical Care

Figure 5

From: Platelet-derived exosomes induce endothelial cell apoptosis through peroxynitrite generation: experimental evidence for a novel mechanism of septic vascular dysfunction

Figure 5

NADPH oxidase and uncoupled NO synthase are sources of reactive species from platelet-derived exosomes. Exosomes from septic patients, as well as exosomes induced with the nitric oxide donor diethylamine NONOate (NONOate; 0.5 μM) and lipopolysaccharide (LPS) caused enhanced 2',7'-dichlorofluorescein diacetate (10 mM) fluorescence (after the addition of 100 μM NADPH), which was significantly inhibited by the membrane-permeable superoxide dismutase mimetic Mn(III) tetrakis (4-benzoic acid) porphyrin chloride (SOD) or by the NADPH oxidase-blocking peptide gp91 ds-tat (10 μM), confirming the role of a superoxide-generating NADPH oxidase. Nω-nitro-D-arginine methyl ester (L-NAME) decreased the fluorescent signals, suggesting a role for uncoupled nitric oxide synthase in superoxide generation. The scrambled peptide (scr ds-tat) used as a control for gp91 ds-tat shows a non-significant residual inhibitory effect. Results are means ± SD of five experiments for each group. *P < 0.05 versus control, †P < 0.05 versus untreated. RFU, relative fluorescence units.

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