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. 2014 Nov 24;12(6):692–699. doi: 10.1038/cmi.2014.108

Figure 4.

Figure 4

PI3K signaling is important for the RGC-32-mediated induction of IL-6 production. (a) THP-1 cells were exposed to 100 ng/ml PMA for the indicated times. Whole-cell lysates were prepared and subjected to western blot analysis to detect phosphorylated Akt. (b) RGC-32-silenced or control THP-1 cells were treated with LY294002 for 1 h prior to further stimulation with PMA. After 48 h, the production of IL-1β, IL-6, TNF-α and TGF-β in the cell-free supernatants was assayed by ELISA. (c) RGC-32-silenced or control THP-1 cells were exposed to PMA for 48 h. Whole-cell lysates were subjected to western blot analysis to detect phosphorylated Akt. (d) RGC-32 physically interacts with AKT in THP-1 cells and PMA-treated macrophages. THP-1 cells were treated with 0 or 100 ng/ml PMA for 48 h, and subsequently coimmunoprecipitation was performed. Control IgG and AKT antibodies were used for coimmunoprecipitation, and anti-RGC-32 was used for immunoblotting. *P<0.05, **P<0.01. PI3K, phosphoinositide 3-kinase; PMA, phorbol 12-myristate 13-acetate; RGC-32, response gene to complement 32.