Figure 3.

SGK1 inhibition promotes Porphyromonas gingivalis–mediated NF-κB activity and c-Jun expression. Human monocytes, pretreated with/without EMD638683 for 2 h (A, C, and D), and BMDMs (B and E) that were generated from LysM-cre-sgk1^fl/fl or littermate control mice were stimulated with P. gingivalis for the time indicated. Whole cell lysates were harvested for Western blotting assay, and the immunoblots were probed with antibodies to p-NF-κB, p-P38, p-ERK, and total c-Jun. The intensity ratio of phosphorylation of NF-κB to total NF-κB was determined by densitometry quantification assay. Antibodies to GAPDH were used as a loading control. A–C, Western blots showing SGK1 inhibition or deficiency enhances P. gingivalis–induced NF-κB activation (A) with densitometry quantification result (A, right panel) but does not affect p-P38 and p-ERK in monocytes (C) and BMDMs (B). D and E, inhibition or SGK1 deficiency leads to a remarkable increase of c-Jun in P. gingivalis–stimulated monocytes (D) and BMDMs (E) (this is the same blot as that for Fig. 4A). All the blots shown are representative of 3 to 5 independent experiments. BMDM, bone marrow–derived macrophage; ERK, extracellular-regulated kinase; SGK1, serum- and glucocorticoid-regulated kinase 1.