Cigarette smoke induces mucin hypersecretion and inflammatory response through the p66shc adaptor protein-mediated mechanism in human bronchial epithelial cells
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- 作者：J. Yanga ; H.M. Yub ; X.D. Zhoua ; c ; zxd999@263.net" class="auth_mail" title="E-mail the corresponding author ; H.P. Huangc ; Zh. Hanc ; V.P. Kolosovd ; J.M. Perelmand
- 关键词：p66Shc ; Mitochondria ; ROS ; NF-κB ; Inflammation ; MUC5AC
- 刊名：Molecular Immunology
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：69
- 期：Complete
- 页码：86-98
- 全文大小：3134 K
文摘
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p66Shc adaptor protein is a newly recognized mediator of mitochondrial dysfunction.
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Expression of p66Shc was significantly increased in human airway epithelial cells with CSE exposure.
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The high expression of p66Shc induced excess of intracellular ROS production and mitochondria dysfunction.
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Excessive ROS triggers the inflammatory response and mucus hypersecretion in part by activating NF-κB signaling and inhibiting FoxO3a activity.
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Manipulating p66Shc might offer a new therapeutic modality with which to treat chronic inflammatory airway diseases.