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. 2013 Dec 24;289(10):6383–6393. doi: 10.1074/jbc.M113.536805

FIGURE 6.

FIGURE 6.

PPARγ activation reverses CSE-induced changes in PPARγ, GR-α, and HDAC2 and in chromatin acetylation. Shown are effects of treatment with Rosi (1 μm) or OA-NO2 (100 nm) followed by CSE treatment (10%, 6 h) of H292 cells. A, Western blots showing nuclear levels of PPARγ, GR-α, and HDAC2, as well as showing acetyl- and phospho-histone H3 (Lys-9/Ser-10) and total histone H3; acetylated (Lys-12) and total histone H4. Veh, vehicle. B, Western blots (IB) showing phosphorylation in immunoprecipitated (IP) PPARγ, acetylation in immunoprecipitated GR-α, and 4-hydroxy-2-nonenal (4-HNE) alkylation, nitrosylation, and phosphorylation in immunoprecipitated HDAC2. C, DNA binding activity of PPARγ. D, DNA binding activity of GR-α. E, deacetylation activity of HDAC. All activities were measured using ELISA-based assays. Data are representative of three independent experiments with n = 3–5. **, p < 0.01, ***, p < 0.001.

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