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. 2015 Jan 27;10(1):e0116773. doi: 10.1371/journal.pone.0116773

Fig 8. Effects of TNF and formoterol on gene expression induced by NR3C1 ligands.

Fig 8

BEAS-2B cells were pre-treated for 1 h with 10 ng/ml of tumor necrosis factor-α (TNF), prior to the addition of 10 nM formoterol (Form) and/or the NR3C1 ligands: 1 μM dexamethasone (Dex), 100 nM fluticasone furoate (FF), 100 nM des-ciclesonide (DC) or 100 nM GW870086X (GW). Cells were harvested 6 h after NR3C1 ligand addition. Total RNA was extracted, cDNA synthesized and RT-PCR performed for: cyclin-dependent kinase inhibitor 1C (CDKN1C; p57KIP2), dual specificity phosphatase 1 (DUSP1; MKP1), regulator of G-protein signaling 2 (RGS2), TSC22 domain family member 3 (TSC22D3; GILZ) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Data (n = 5), normalized to GAPDH, are expressed as fold and plotted as means ± S.E. Statistical significance was tested using repeated measures, one-way analysis of variance (ANOVA) with Bonferroni’s correction for multiple comparisons. *, P<0.05; **, P<0.01; ***, P<0.001. Each NR3C1 ligand significantly increased expression of all four genes.