title: The mechanism of UVB irradiation induced-apoptosis in cataract.
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.
authors.affiliation: Department of Ophthalmology, Eye & ENT Hospital of Fudan University, No. 83 Fenyang Road, Shanghai, 200031, China.
authors.forename: Yinghong
authors.initials: Y
authors.lastname: Ji
authors.forename: Lei
authors.initials: L
authors.lastname: Cai
authors.forename: Tianyu
authors.initials: T
authors.lastname: Zheng
authors.forename: Hongfei
authors.initials: H
authors.lastname: Ye
authors.forename: Xianfang
authors.initials: X
authors.lastname: Rong
authors.forename: Jun
authors.initials: J
authors.lastname: Rao
authors.forename: Yi
authors.initials: Y
authors.lastname: Lu
mesh_terms: D017209:Apoptosis / Q000528:radiation effects*; D002386:Cataract / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002460:Cell Line; D004847:Epithelial Cells / Q000166:cytology / Q000528:radiation effects; D005786:Gene Expression Regulation / Q000528:radiation effects; D006801:Humans; D007908:Lens, Crystalline / Q000473:pathology*; D053078:Membrane Potential, Mitochondrial / Q000528:radiation effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D011832:Radiation Injuries / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000528:radiation effects; D015398:Signal Transduction / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: C494826:BAX protein, human; C000595707:BCL2 protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein