@misc{oai:niigata-u.repo.nii.ac.jp:00005800,
 author = {Oyanagi, Takahito},
 month = {Sep},
 note = {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 MUC5AC expression is regulated by a variety of stimuli such MUC5AC expression is regulated by a variety of stimuli such MUC5AC expression is regulated by a variety of stimuli such 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-γin 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 signale-regulated kinase(ERK). A chromatin immunoprecipitation assay indicated that Sp1 bound to its cognate sequence located on the MUC5AC promoter. The Sp1inhibitor 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., 学位の種類: 博士（医学）. 報告番号: 甲第4212号. 学位記番号: 新大院博（医）甲第711号. 学位授与年月日: 平成28年9月20日, 新大院博（医）甲第711号},
 title = {Suppression of MUC5AC expression in human bronchial epithelial cells by interferon-γ},
 year = {2016}
}