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L. Wang, R. Peyton, L. Lu; Hyperosmotic Stress-induced Plk3 Activation in Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2591.
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The purpose of the study is to investigate hyperosmotic stress-induced activation of c-Jun/AP-1 through a novel Polo-like kinase 3 (Plk3) pathway in human corneal epithelial cells.
Human corneal epithelial (HCE) cells were cultured in DMEM/F12 medium containing 10% FBS and 5 µg/ml insulin at 37°C, 5% CO2. Hyperosmotic stress was applied with various concentrations of sorbitol to cultured cells for 1 h. Immunoprecipitation and kinase assays were employed to measure hyperosmotic stress-induced Plk3 kinase activity. Cell viability was detected by MTT assay and Immunoblot was performed to analyze the expression of protein with specific antibody.
1) Hyperosmotic stress induced activation of Plk3 in a dose-dependent manner in HCE cells. 2)Cell growth significantly decreased after exposed HCE cells to hyperosmotic stress. 3)Hyperosmotic stress induced site-specific phosphorylation of c-jun at serine 63 and serine 73 in HCE cells. 4) Osmotic stress-induced activation of signaling cascades was detected by measuring p38 activities. 5) Effect of osmotic stress-induced Plk3 activation on cell viability was examined with various assays.
Our results, for the first time, provide a novel signaling mechanism that involves hyperosmotic stress-induced activation of Plk3 pathway in addition to p38 MAPK pathway to deregulate c-Jun activity resulting in control of HCE cell proliferation and apoptosis.
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