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. Author manuscript; available in PMC: 2016 Mar 18.
Published in final edited form as: Free Radic Biol Med. 2013 Oct 2;65:1331–1339. doi: 10.1016/j.freeradbiomed.2013.09.027

Figure 5. STAT3 is required for HO-1-induced TTP expression in macrophages.

Figure 5

(A–C) Nicotine-HO-1 enhances STAT3 phosphorylation. (A) RAW 264.7 cells were treated with 1 mM nicotine for the indicated times and the levels of total STAT3 and phospho-STAT3 were analyzed by Western blot assays. (B) RAW 264.7 cells were pretreated with 20 μM ZnPP for 30 min and further incubated with the indicated concentration of nicotine for 24 h. The levels of total STAT3 and phospho-STAT3 were analyzed by Western blot assays. (C) RAW 264.7 cells were transfected with HO-1-siRNA. After treatment with 1 mM nicotine for 24 h, the levels of STAT3, phospho-STAT3, and HO-1 were analyzed by Western blot assays. (D) Peritoneal macrophages were harvested from HO-1 KO and wild-type mice. Cells were treated with 1 mM nicotine for 24 h. The level of HO-1, STAT3, and phospho-STAT3 were determined by Western blot assays. (E–H) STAT3 is required for nicotine-induced TTP expression. RAW 264.7 cells were transfected with STAT3-siRNA. (E) The level of STAT3 was analyzed by Western blot assays. (F) Cells were incubated with 10μM CoPP for 18h and the levels of TTP, HO-1, and STAT3 were analyzed by semi-qRT-PCR. (G) After treatment with 1 mM nicotine for 24 h, the levels of TTP, STAT3, and HO-1 were analyzed by semi-qRT-PCR. (H) After treatment with 1 mM nicotine and 1 μg/ml LPS for 24 h, the levels of TTP, STAT3, HO-1, and TNF-α were analyzed by semi-qRT-PCR.