Role of NADH: quinone oxidoreductase-1 in the tight junctions of colonic epithelial cells

BMB Reports

Dae Hong Kim^1¹  Mi Jung Park^1²  Seung Taek Nam^1³  Jung Hwan Hwang^2⁴ 

[1] Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Suwon 441-707^3;Department of Internal Medicine, Chungnam National University, Daejon 301-721, Korea^4;Department of Life Science, College of Natural Science, Daejin University, Pocheon 487-711^1;Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 305-806^2

关键词: Barrier dysfunction of epithelial cells;   

DOI  :  

学科分类：生物化学/生物物理

来源: Korean Society for Biochemistry and Molecular Biology

【 摘 要 】

NADH:quinone oxidoreductase 1 (NQO1) is known to be involved in the regulation of energy synthesis and metabolism, and the functional studies of NQO1 have largely focused on metabolic disorders. Here, we show for the first time that compared to NQO1-WT mice, NQO1-KO mice exhibited a marked increase of permeability and spontaneous inflammation in the gut. In the DSS-induced colitis model, NQO1-KO mice showed more severe inflammatory responses than NQO1-WT mice. Interestingly, the transcript levels of claudin and occludin, the major tight junction molecules of gut epithelial cells, were significantly decreased in NQO1-KO mice. The colons of NQO1-KO mice also showed high levels of reactive oxygen species (ROS) and histone deacetylase (HDAC) activity, which are known to affect transcriptional regulation. Taken together, these novel findings indicate that NQO1 contributes to the barrier function of gut epithelial cells by regulating the transcription of tight junction molecules.

【 授权许可】

Unknown