期刊
SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep13262
关键词
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资金
- Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) [26112713, 25711012, 24657131]
- Kao Foundation for Arts and Sciences
- Heiwa Nakajima Foundation
- Takeda Science Foundation
- Astellas Foundation
- Senri Life Science Foundation
- Inamori Foundation
- Nakatomi Foundation
- Daiichi Sankyo Foundation of Life Science
- Kanae foundation
- Fukuoka Foundation for Sound Health Foundation
- Ono Medical Research Foundation
- Cosmetology Research Foundation
- Grants-in-Aid for Scientific Research [24657131, 25711012, 26112713] Funding Source: KAKEN
Epithelial cells define the boundary between the outside and the inside of our body by constructing the diffusion barrier. Tight junctions (TJs) of epithelial cells function as barriers against invasion of harmful microorganisms into the human body and free diffusion of water or ions from the body. Therefore, formation of TJs has to be strictly controlled in epithelial cells. However, the molecular mechanisms governing this regulation are largely unknown. In this study, we identified Ca2+/calmodulin-dependent protein kinase II (CaMKII) as a regulator of the barrier function of TJs. CaMKII inhibition led to enlargement of TJ-areas and up-regulation of the barrier function. CaMKII inhibition induced excess TJ formation in part by the activation of AMP-activated protein kinase (AMPK) and subsequent phosphorylation of claudin-1. As up-regulation of epithelial barriers is essential for the prevention of chronic inflammatory diseases, the identification of CaMKII as a modulator of TJ function paves the way for the development of new drugs to treat these diseases.
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