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Published on: June 14, 2016
Suppression of MUC5AC expression in human bronchial epithelial cells by interferon-γ
Takahito Oyanagi1, Takumi Takizawa2, Akira Aizawa2
1Department of Pediatrics, Graduate School of Medicine, Gunma University, Gunma, Japan; Department of Pediatrics, Graduate School of Medicine, Niigata University, Niigata, Japan.
Background:
Excessive mucin secretion in the airway is an important feature of airway inflammatory diseases. MUC5AC expression is regulated by a variety of stimuli such as cytokines. Little is known about the role of interferon (IFN)-γ in MUC5AC expression in human bronchial epithelial cells.
Methods:
Human pulmonary mucoepidermoid carcinoma cell line (NCI-H292) and normal human bronchial epithelial (NHBE) cells were used to assess the effects of IFN-γ on MUC5AC transcription.
Results:
Transforming growth factor (TGF)-α and double-stranded RNA (polyI:C)-induced MUC5AC mRNA and protein expression was repressed by IFN-γ in a concentration-dependent manner. IFN-γ showed limited effects on TGF-α and polyI:C-induced activation of epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase (ERK). A chromatin immunoprecipitation assay indicated that Sp1 bound to its cognate sequence located on the MUC5AC promoter. The Sp1 inhibitor mithramycin A inhibited MUC5AC mRNA expression, implying a critical role for Sp1 in MUC5AC induction. Importantly, IFN-γ impeded Sp1 binding to the MUC5AC promoter.
Conclusions:
These results suggest that IFN-γ represses MUC5AC expression, disturbing binding of Sp1 to its target sequences.
