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. 2015 Jul 24;25(8):893–910. doi: 10.1038/cr.2015.87

Figure 5.

Figure 5

AP1 mediates the proinflammatory gene expression of M(Na) and high-salt-induced potentiation of M(LPS). (A) High salt promotes cFos phosphorylation in macrophages. BMDMs were treated with or without additional 51 mM NaCl for the indicated time periods. p-cFos and total cFos (cFos) levels were measured and GAPDH was used as a loading control. (B) SR inhibits high-salt-promoted proinflammatory gene expression. BMDMs were pretreated with 10 μM SR or DMSO for 1 h and then treated with or without additional 51 mM NaCl for 24 h in the continued presence of 10 μM SR or DMSO. (C) High salt-induced increase of p-cFos depends on p38 activation. BMDMs were pretreated with 10 μM SB for 2 h and then treated with or without additional 51 mM NaCl for 12 h in the presence of 5 μM SB or DMSO. (D) High salt-induced increase of cFos phosphorylation depends on Erk1/2 activation. BMDMs were pretreated with 20 μM PD for 1 h and then treated with or without additional 51 mM NaCl for 12 h in the presence of 20 μM PD or DMSO. (E) High salt enhances LPS-induced p-cFos. BMDMs were treated with or without additional 51 mM NaCl for 13 h and 100 ng/ml LPS was added during the last 1 h of the treatment. (F, G) AP1 mediates high-salt-enhanced response to LPS. BMDMs were treated by the same procedure as in B, except that 100 ng/ml LPS was added to all groups during the last 12 h of the treatment. Expression of the indicated genes (F) and proteins (G) was quantified. (H) High salt-induced increase of p-cFos in the presence of LPS depends on p38 activation. BMDMs were treated by the same procedure as in C, except that 100 ng/ml LPS was added to all groups during the last 1 h of the treatment. For all panels, gene expression was measured using qRT-PCR and protein expression or phosphorylation was measured using western blotting. ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001.