@misc{oai:repo.qst.go.jp:00068532,
 author = {Katsube, Takanori and Tsuji, Hideo and Onoda, Makoto and 勝部 孝則 and 辻 秀雄 and 小野田 眞},
 month = {Jun},
 note = {Tight junctions (TJ) seal adjacent epithelial cells and prevent the apical-basolateral transport of solutes. Reactive oxygen species have been shown to mediate significant increase in epithelial solute permeability and implicated in a wide range of disease processes such as inflammation. We demonstrate here that NO protects against hydrogen peroxide (H2O2)-induced damage of TJ in human intestinal (Caco-2) epithelial cells. The effects of H2O2 and NO on a barrier function of Caco-2 monolayer grown on permeable supports were evaluated by the transepithelial electrical resistance and the paracellular permeability to fluorescein-dextran (3 kDa). Morphological integrity of TJ was investigated by the immunostaining of a scaffolding protein ZO-1. Treatment with H2O2 (36-600 mM) resulted in a deterioration of barrier function and a disruption of morphological organization of TJ. Treatment with NOC5, an NO donor, slightly enhanced the barrier function, though the alteration of ZO-1 localization was not detected. A simultaneous addition of H2O2 (36 mM) and NOC5 (15 mM) to the monolayers showed that NO reduced the damages on barrier function and morphology of TJ induced by H2O2. Western blots using anti-phosphotyrosine antibody revealed that H2O2 stimulated tyrosine phosphorylation of multiple cellular proteins and that NO reduced H2O2-induced protein phosphorylation. The molecular mechanisms underlying modulation of epithelial TJ by H2O2 and NO will be discussed., 20th IUBMB International Congress of Biochemistry and Molecular Biology},
 title = {Nitric oxide protects against hydrogen peroxide-induced damage on epithelial tight junctions.},
 year = {2006}
}