DNA Hypermethylation of in Ultraviolet-B-induced Age-related Cataract Models and
Overview
Affiliations
Aim: To explore the DNA methylation of in ultraviolet-B (UVB)-induced age-related cataract (ARC) models and .
Methods: Human lens epithelium B3 (HLEB3) cells and Sprague Dawley rats were exposure to UVB respectively. The MTT assay was utilized to evaluate cell proliferation. Flow cytometry was employed for analysis of cell apoptosis and cell cycle. expression in HLEB3 cells and anterior lens capsules were assessed using Western blot and reverse transcription-polymerase chain reaction (RT-PCR). The localization of in HLEB3 cells was determined by immunofluorescence. The methylation status of CpG islands located in promoter was verified using bisulfite-sequencing PCR (BSP). DNMTs and TETs mRNA levels was examined by RT-PCR.
Results: UVB exposure decreased HLEB3 cells proliferation, while increased the apoptosis rate and cells were arrested in G0/G1 phase. expression was markedly inhibited in UVB treated cells compared to the controls. Hypermethylation status was detected in the CpG islands within promoter in HLEB3 cells subjected to UVB exposure. Expressions of DNMTs including DNMT1/2/3 were elevated in UVB treated HLEB3 cells compared to that in the controls, while expressions of TETs including TET1/2/3 showed the opposite trend. Results from the UVB treated rat model further confirmed the decreased expression of , hypermethylation status of the CpG islands at promoter of and abnormal expression of DNMT1/2/3 and TET1/2/in UVB exposure group.
Conclusion: DNA hypermethylation of promoter CpG islands is correlated with decreased expression in UVB induced HLEB3 cells and anterior lens capsules of rats.