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Shan Huang, Xialin Liu, Mingxing Wu, Lixia Luo, Zhenzhen Liu, Liqiong Zhu, Baoxin Chen, Fangyuan Liu, Xuhua Tan, Yizhi Liu; Inhibition of α-tubulin deacetylase prevents the migration of lens epithelial cells without affecting cell cycle progression. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1220.
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© ARVO (1962-2015); The Authors (2016-present)
Proliferation and migration of residual lens epithelial cells are causally associated with posterior capsular opacification, the most common complication of modern cataract surgery. The objective of this work is to investigate the effects of α-tubulin deacetylase on the migration and cell cycle progression of lens epithelial cells.
The human lens epithelial cells (HLECs), SRA01/04, were treated with tubacin, an α-tubulin deacetylase inhibitor, at various concentrations (2μM, 5μM and 10μM) for 24-48 hours. The acetylated α-tubulin levels were detected by western blot. The effect of tubacin on cell cycle of HLECs was quantified by flow cytometry analysis. Cell migration was determined by scratch-wound assay. The confluent monolayers of HLECs were treated with tubacin for 24 hours and then scratched with pipette tips. The scratch margins were photographed 0, 4, 18, 24, 28 and 32 hours thereafter to monitor the closure of the scratch. The extend cell migration was determined by comparing the distances between scratch edges at the indicated time points with the initial scratch distance.
The acetylated α-tubulin levels in HLECs were significantly increased after treatment with various concentrations of tubacin, especially in the 10μM-tubacin-treated group. Flow cytometry analysis showed that treatment with tubacin had little effect on the cell cycle progression of HLECs. Scratch wound assay showed that the migration of HLECs was inhibited by tubacin treatment. At 32 hours after scratch, the cell migration was inhibited 10%, 29% and 41%, respectively, when the cells were treated with 2μM, 5μM and 10μM tubacin.
Tubacin, an α-tubulin deacetylase inhibitor, could inhibit the migration of HLECs without affecting the cell cycle progression, indicating that α-tubulin deacetylase is a potential drug target for the prevention and treatment of posterior capsular opacification.
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