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L. Wang, R. Peyton, L. Lu; Hyperosmotic Stress-Induced ATF-2 Activation Mediated by Plk3 in Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1975.
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© ARVO (1962-2015); The Authors (2016-present)
Hyperosmotic stress-induced p38 MAPK pathway plays important role in human corneal epithelial (HCE) migration in wound healing. The purpose of this study is to investigate, in addition to the p38 pathway, the role of Polo-like kinase 3 (Plk3) in mediating hyperosmotic stress-induced activation of ATF-2 in HCE cells.
HCE cells were cultured in DMEM/F12 medium containing 10% FBS and 5 µg/ml insulin at 37°C with 5% CO2. Hyperosmotic stress was deployed by applying various concentrations of sorbitol to cells. Western blot was performed to analyze expression of the targeting protein. Immunoprecipitation and kinase assays were employed to measure hyperosmotic stress-induced Plk3 kinase activity.
We found that Plk3 plays a functional role in mediating stress-induced cellular responses. Our results demonstrated in HCE cells: 1) hyperosmotic stress-induced Plk3 activation is correlated to ATF-2 activation in a dose-dependent manner; 2) there was a protein-protein interaction between Plk3 and ATF-2; 3) Plk3 directly phosphorylated ATF-2at the site of Thr-71; 4) knockdown of Plk3 by using specific siRNA diminished stress-induced ATF-2 phosphorylation; and 5) over-expression of Plk3 enhanced hyperosmotic stress-induced ATF-2 activation.
Plk3 is a stress-induced protein kinase and plays an important role in hyperosmotic stress-induced activation of ATF-2 in addition to MAPK pathways in HCE wound healing.
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