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

Fig 7. Effects of JNK MAPK or IKK2 inhibition on TNF-induced repression of glucocorticoid inducible gene expression.

Fig 7

BEAS-2B cells were pre-treated for 30 min with either 10 or 3 μM of the JNK MAPK inhibitor JNK inhibitor VIII (JNK) or 10 μM of the IKK2 inhibitor PS-1145 (PS), before addition of 10 ng/ml tumor necrosis factor-α (TNF). After 1 h, 1 μM dexamethasone (Dex) and/or 10 nM formoterol (Form) was added and cells were harvested 6 h later. 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 = 9), normalized to GAPDH, are expressed as fold and plotted as means ± S.E. Significance was tested using repeated measures, one-way analysis of variance (ANOVA) with Bonferroni’s correction for multiple comparisons. **, P<0.01. Dexamethasone significantly increased expression of all four genes.