Fig. 3.

DCA induces AKT-independent activation of p38 MAPK. A) DCA-activated cellular signaling in VSMC. Wild type VSMC were serum starved and then treated with 5 mM DCA for different durations. Phosphorylation/activation of AKT, ERK1/2 and p38 MAPK signals was determined by Western blotting analysis. a) Representative blots from 3 independent experiments are shown. The expression of β-actin was used as a loading control. b) Quantification of pp38 MAPK and pERK1/2, normalized by β-actin (n = 3, *p < 0.05). B) and C) DCA-activated signals in mouse aortas. B) Immunofluorescent analysis of phosphorylation/activation of AKT and p38 MAPK MAPK in consecutive aortic root sections. a) Representative images (scale bar= 500 µm). b) and c) Quantification analysis of pAKT and pp38 MAPK in a). (n = 9, * *p < 0.001). C) Western blot analysis of phosphorylation/activation of AKT and p38 MAPK in descending aorta from mice with or without DCA treatment. D) Effects of inhibition of either AKT or p38 MAPK on DCA-induced AKT/p38 MAPK activation. VSMC were serum starved, pretreated with the inhibitors for p38 MAPK (SB203580, 10 µM) or AKT (AKT IV, 0.1 µM), and subsequently exposed to 5 mM DCA for 10 min. The activation of AKT and p38 MAPK was determined by Western blotting analysis. Representative blots from 3 independent experiments are shown.