Fig. 8.

Mechanistic pathways involved in corticosteroid resistance of Muc1 KO mice. C57BL/6 Muc1 KO mice and WT mice were undergoing intranasal instillation of 75 μg of lipopolysaccharide (LPS) at day 1. Between days 2 and 3, animals were exposed to cigarette smoke (or control air) of 6 cigarettes followed by 8 cigarettes (or control air) at days 4 and 5, and 10 cigarettes (or control air) at day 6. Vehicle or dexamethasone at 3 mg/kg/day and 10 mg/kg/day was administered orally once a day between day 1 and 6. Animals were sacrificed at day 6 and lungs were homogenized to analyze protein expression of (a) glucocorticoid receptor alpha (GRα), (b) GR phosphorylated at ser226 (GR-ser²²⁶), (c) Muc1 cytoplasmic tail (CT), (d) phospho-p38 and (e) phopho-ERK1/2. Protein expression was normalized to β-actin. f Representative western blots are showed. Results are the mean ± SE of n = 8 animals per experimental group. One-way ANOVA followed by Bonferroni post-hoc tests. *P < 0.05 compared with control. #P < 0.05 compared with LPS/ LPS + CS. KO: knock out; WT: wild type; CS: cigarette smoke; LPS: lipopolysaccharide