2017年1月
Suppression of MUC5AC expression in human bronchial epithelial cells by interferon-γ.
Allergology international : official journal of the Japanese Society of Allergology
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- 巻
- 66
- 号
- 1
- 開始ページ
- 75
- 終了ページ
- 82
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.alit.2016.05.005
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.
- リンク情報
- ID情報
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- DOI : 10.1016/j.alit.2016.05.005
- PubMed ID : 27324793