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Publication : Nox2-derived ROS in PPARγ signaling and cell-cycle progression of lung alveolar epithelial cells.

First Author  Tickner J Year  2011
Journal  Free Radic Biol Med Volume  51
Issue  3 Pages  763-72
PubMed ID  21664456 Mgi Jnum  J:174696
Mgi Id  MGI:5140639 Doi  10.1016/j.freeradbiomed.2011.05.027
Citation  Tickner J, et al. (2011) Nox2-derived ROS in PPARgamma signaling and cell-cycle progression of lung alveolar epithelial cells. Free Radic Biol Med 51(3):763-72
abstractText  Reactive oxygen species (ROS) play important roles in peroxisome proliferator-activated receptor gamma (PPARgamma) signaling and cell-cycle regulation. However, the PPARgamma redox-signaling pathways in lung alveolar epithelial cells remain unclear. In this study, we investigated the in vivo and in vitro effects of PPARgamma activation on the levels of lung ROS production and cell-cycle progression using C57BL/6J wild-type and Nox2 knockout mice (n=10) after intraperitoneal injection of a selective PPARgamma agonist (GW1929, 5 mg/kg body wt, daily) for 14 days. Compared to vehicle-treated mice, GW1929 increased significantly the levels of ROS production in wild-type lungs, and this was accompanied by significant up-regulation of PPARgamma, Nox2, PCNA, and cyclin D1 and phosphorylation of ERK1/2 and p38MAPK. These effects were absent in Nox2 knockout mice. In cultured alveolar epithelial cells, GW1929 (5 muM for 24 h) increased ROS production and promoted cell-cycle progression from G0/G1 into S and G2/M phases, and these effects were abolished by (1) adding a PPARgamma antagonist (BADGE, 1 muM), (2) knockdown of PPARgamma using siRNA, or (3) knockout of Nox2. In conclusion, PPARgamma activation through Nox2-derived ROS promotes cell-cycle progression in normal mouse lungs and in cultured normal alveolar epithelial cells.
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