Purchase this article with an account.
N. Kasaoka, T. Inoue, T. Kameda, T. Fujimoto, M. Inoue-Mochita, H. Tanihara; The Response to Trabecular Meshwork Cells for Oxidative Stress Mediated by Akt Activation. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3230.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the response of trabecular meshwork (TM) cells against oxidative stress.
After overnight serum starvation, cultured porcine TM cells were treated with hydrogen peroxide (H2O2) at 600 µM or 800 µM, and their time-dependent morphological changes were observed by microscope. Akt phosphorylation was evaluated by Western blot using antibody against phosphorylated Akt (Ser473) after H2O2 treatment time dependently. Pretreatment with LY294002, Akt inhibitor IV, DHMEQ, an inhibitor of phosphatidylinositol-3 kinase (PI3K), Akt, nuclear factor ΚB (NFΚB), respectively, were also conducted to address the effect of H2O2 treatment on intracellular signaling.
TM cells represented abnormal morphology with shrinkage at 2 hours of H2O2 treatment, and then recovered time-dependently. The ratio of pAkt in total Akt represented 3.8 (p=0.016), 2.4 and 1.5 fold increases compared with control at 20, 40 and 60 minutes, respectively, after treatment with H2O2 at 600 µM. The recovery of cell morphology was inhibited by pretreatment of each inhibitor described above.
TM cells are indicated to recover from the morphological alteration associated with oxidative stress by activation of PI3K-Akt-NFΚB signaling pathway.
This PDF is available to Subscribers Only