Figure 3.

Effects of S-MSC treatment on cytokine release in the plaque of brachiocephalic arteries of apolipoprotein E-knockout mice. Representative sections from eight mice are shown. (A, B): Immunofluorescent staining of cryosections of the three groups (Fig. 1) of mouse atherosclerotic plaques with either goat anti-mouse TNF-α (primary antibody)/Alexa Fluor 555 donkey anti-goat IgG (H+L) (secondary antibody) (A), or rat anti-mouse IL-10 (primary antibody)/Alexa Fluor 555 goat anti-rat IgG (H+L) (secondary antibody) (B). Cell nuclei were counterstained with DAPI (blue). The accumulation of TNF-α was significantly decreased and IL-10 was increased in the plaques in mice treated with wild-type S-MSCs compared with AS mice, but not for KO-S-MSCs. Graphs show quantification of TNF-α and IL-10 in the plaque area of the three groups. All results are representative of the arithmetic mean ± SEM of eight independent experiments. ∗∗, p < .01 versus AS. Scale bars = 100 µm. Original magnifications, ×100 (main panels) and ×400 (insets). Abbreviations: AS, atherosclerosis; DAPI, 4′,6-diamidino-2-phenylindole; IL-10, interleukin 10; KO-S-MSCs, nuclear factor-κB^−/− skin-derived mesenchymal stem cell treatment group; ns, nonsignificant; S-MSC, skin-derived mesenchymal stem cell; TNF-α, tumor necrosis factor-α.