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. 2018 Jul 5;39(11):1725–1734. doi: 10.1038/s41401-018-0072-0

Fig. 6.

Fig. 6

Fig. 6

ClC-3 increased p47phox phosphorylation through p38 MAPK pathway. a The time course of p47phox and p38 MAPK phosphorylation in Ang II-treated HUVECs (n = 5, *P < 0.05 vs. CON, **P < 0.01 vs. CON). b Knockdown of ClC-3 decreased p38 MAPK phosphorylation induced by Ang II (1 μmol/L) treatment for 30 min. c Overexpression of ClC-3 enhanced p38 MAPK phosphorylation (n = 5, *P < 0.05 vs. CON, #P < 0.05 vs. Ang II). d–f Cells were pretreated with the p38 MAPK inhibitor SB203580 (10 μmol/L) for 6 h before Ad-ClC-3 transfection. SB203580 abolished the increase in p47phox phosphorylation (d), NADPH oxidase activity (e), and ROS generation (f) induced by ClC-3 overexpression in HUVECs with Ang II treatment, respectively (n = 6, **P < 0.01 vs. Ang II, ##P < 0.01 vs. Ang II+Ad-ClC-3)