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The mechanism of UVB irradiation induced-apoptosis in cataract

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Abstract

Cataract is the most common eye disease that causes blindness in patients. Ultraviolet B (UVB) irradiation is considered an important factor leading to cataract by inducing apoptosis in human lens epithelial cells (HLECs), but the mechanism is currently unclear. In this study, we investigated HLECs under different intensities of UVB irradiation and different exposure time. The annexin V-FITC/propidium iodide staining results showed that UVB irradiation could efficiently lead to HLECs apoptosis in time- and dose-dependent manner. The expression of pro-apoptotic Bax gene was promoted by UVB irradiation, while anti-apoptotic Bcl-2 gene expression was inhibited at both transcript and protein levels. Notably, the ratio of Bax/Bcl-2 displayed a high and positive correlation to the proportion of apoptotic HLECs. Mitochondrial dysfunction was also observed with rapid loss of potential (∆Ψ m), as well as changes of the levels of reactive oxygen species, malondialdehyde, total antioxidative capabilities, and superoxide dismutase. In caspase pathway, the level of caspase-3 protein increased after UVB irradiation. All these discovered changes may play important roles in UVB-induced HLECs apoptosis, and would be helpful in understanding the mechanism of UVB-induced cataract and providing potential prevention and treatment strategies.

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Acknowledgments

This work was supported by Grant No. 81300745 from National Science Foundation of China, Grant No. 11231200602 from Shanghai Science and Technology Commission and Grant No. PW 2011D-7 from Key-Collaborative Project of Health Bureau of Pudong New Area.

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The authors declare no competing financial interest.

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Correspondence to Yi Lu.

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Yinghong Ji and Lei Cai have contributed equally to this work.

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Ji, Y., Cai, L., Zheng, T. et al. The mechanism of UVB irradiation induced-apoptosis in cataract. Mol Cell Biochem 401, 87–95 (2015). https://doi.org/10.1007/s11010-014-2294-x

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  • DOI: https://doi.org/10.1007/s11010-014-2294-x

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