Abstract
Purpose
Cataract is a leading visual disease characterized by enhanced oxidative stress and increased apoptosis of human lens epithelial cells (HLECs). TRIM3 is a tumor suppressor in many cancers. However, its role in cataract remains unknown. In this study, we aimed to explore the role of TRIM3 in H2O2-injured HLECs and the underlying mechanisms involved.
Methods
HLECs were treated with different H2O2 concentrations to induce apoptosis. A lentivirus was designed to overexpress TRIM3 and p53, and TRIM3 knockdown was prepared. A P53 inhibitor, PFTα, was used to knockdown p53. Cell viability and apoptosis were detected by CCK-8 and flow cytometric analyses, respectively. TRIM3, p53, Bcl2, and Bax expression levels were determined by qRT-qPCR and western blotting.
Results
It was found that H2O2-treated HLECs had markedly decreased cell viability and TRIM3 expression. TRIM3 overexpression attenuated the H2O2-induced HLEC apoptosis, while TRIM3 knockdown promoted it. P53, a downstream target of TRIM3, was found to be negatively regulated by TRIM3 via ubiquitination in HLECs. Furthermore, p53 overexpression abolished the effect of TRIM3 overexpression on H2O2-induced HLEC apoptosis, while PFTα alleviated the TRIM3 knockdown-mediated HLEC apoptosis.
Conclusion
This study demonstrates that TRIM3 inhibited the H2O2-induced apoptosis of HLECs by decreasing p53 via ubiquitination.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data that support the findings of this study are available from the corresponding author CW upon reasonable request.