T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells

Figure 5

Oxidative stress induced in cMVECs by CD4-exosomes is regulated by ERK1/2 and MEK1/2 pathway. cMVECs were stimulated for 16 h with CD4-exosomes (CD4 Exo) in the presence or absence of ERK1/2 inhibitor (FR180204), MEK1/2 inhibitor (U0126), and NOX inhibitor (GKT136901). Panels (a)–(e) show effect of indicated treatment on total ROS levels (a), , mitochondrial ROS generation (b), , NO bioavailability (c), , peroxynitrite levels (d), , and cell proliferation (e), . , , and calculated by one-way ANOVA followed by Fisher’s LSD post hoc test versus control group or for indicated groups.

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