CaMKII regulates the strength of the epithelial barrier

Ryo Shiomi, Kenta Shigetomi, Tetsuichiro Inai, Masami Sakai, Junichi Ikenouchi

研究成果: Contribution to journalArticle査読

16 被引用数 (Scopus)

抄録

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.

本文言語英語
論文番号13262
ジャーナルScientific reports
5
DOI
出版ステータス出版済み - 8 18 2015

All Science Journal Classification (ASJC) codes

  • 一般

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