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. 2010 Dec 14;286(7):5823–5835. doi: 10.1074/jbc.M110.192393

FIGURE 6.

FIGURE 6.

Nitric oxide-dependent and -independent signaling cascades regulate NOD2-triggered COX-2 expression. A, mouse macrophages were pretreated with PP2 followed by treatment with MDP and analysis of the activation status of PKC, ERK1/2, and p38 MAPK by immunoblotting. B, pan-PKC inhibitors RO31-8220 and chelerythrine as well as isoform-specific inhibitors of PKC abolished the MDP-triggered COX-2 expression. C, analysis of the MDP-triggered COX-2 expression upon pretreatment of macrophages with ERK1/2 inhibitor, U0126; p38 MAPK inhibitor; JNK1/2 inhibitor, SP600125. D, pretreatment with the pan-PKC inhibitor chelerythrine abrogated MDP-triggered activation of ERK1/2 and p38 MAPK. E, analysis of MDP-induced activation of PKC, ERK1/2, and p38 MAPK in macrophages derived from WT and iNOS−/− mice. F, nuclear localization of p65 NF-κB in MDP-treated WT macrophages, with or without pretreatment with PP2, GSI-I, or LY294002, or chelerythrine, U0126, or p38 MAP kinase inhibitor as well as in macrophages derived from iNOS−/− mice. The blots are representative of three independent experiments. Med, medium.