Journal Article

Gaseous Nitrogen Oxides Stimulate Cell Cycle Progression by Rubidium Phosphorylation via Activation of Cyclins/Cdks

Jing-Hsien Chen, Tsui-Hwa Tseng, Yung-Chyan Ho, Hui-Hsuan Lin, Wea-Lung Lin and Chau-Jong Wang

in Toxicological Sciences

Volume 76, issue 1, pages 83-90
Published in print November 2003 | ISSN: 1096-6080
Published online November 2003 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/kfg221
Gaseous Nitrogen Oxides Stimulate Cell Cycle Progression by Rubidium Phosphorylation via Activation of Cyclins/Cdks

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Nitrogen oxides (NOx) are important indoor and outdoor air pollutants. Many studies have indicated that NOx gas causes lung tissue damage by its oxidation properties and its free radicals. In a previous study we demonstrated that NOx gas induced proliferation of human lung fibroblast MRC-5 cells. In this study we show that NOx gas stimulates MRC-5 cell proliferation by Rb (rubidium) phosphorylation via activation of cyclin-cell division protein kinase (cdk) complexes. Western blot and immunoprecipitation data showed that NOx gas increased the expressions of cyclinA/cdk2, cyclinD1/cdk4, and cyclinE/cdk2 complexes in the cells at 9 h after treatment. The levels of phospho-Rb were also increased and cdk inhibitors (CKIs) p27 and p16 were apparently decreased. These data suggested that NOx gas stimulates cell-cycle progression by Rb phosphorylation via activation of cyclin-cdk complexes and inhibition of CKIs. In conclusion, the NOx-gas that induced lung fibroblast cell proliferation by stimulation of cell-cycle progression may contribute to lung fibrosis by NOx pollutants.

Keywords: gaseous nitrogen oxides; proliferation; cdk inhibitor (CKI); Rb phosphorylation; cell cycle progression

Journal Article.  4674 words.  Illustrated.

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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