These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Long non-coding RNA ANRIL alleviates H2O2-induced injury by up-regulating microRNA-21 in human lens epithelial cells.
    Author: Du S, Shao J, Qi Y, Liu X, Liu J, Zhang F.
    Journal: Aging (Albany NY); 2020 Apr 20; 12(8):6543-6557. PubMed ID: 32310822.
    Abstract:
    The accurate role of ANRIL in cataract is poorly understood. We aimed to reveal the effects of ANRIL on H2O2-treated HLECs, SRA01/04, as well as the regulatory mechanisms. Oxidative stress model of HLECs was induced by H2O2. Cell injury was evaluated according to cell proliferation, apoptosis and DNA damage using CCK-8 assay/flow cytometry and TUNEL assays/γH2AX staining. Expressions of ANRIL and miR-21 in HLECs were determined by RT-qPCR. The effects of miR-21, miR-34a and miR-122-5p inhibition as well as AMPK and β-catenin on HLECs with ANRIL overexpression and H2O2 stimulation were analyzed. In vivo experiment was performed via RT-qPCR. H2O2 repressed proliferation and induced apoptosis or DNA damage in HLECs. Those alterations induced by H2O2 were attenuated by ANRIL overexpression. MiR-21 was positively regulated by ANRIL, and both of them were repressed in H2O2-induced HLECs and cataract patient tissues. Inhibition of miR-21 but not miR-34a or miR-122-5p reversed the effects of ANRIL on H2O2-treated HLECs. Phosphorylation of AMPK and expression of β-catenin were increased by ANRIL via regulating miR-21. AMPK and β-catenin affected beneficial function of ANRIL-miR-21 axis.Therefore, lncRNA ANRIL attenuated H2O2-induced cell injury in HELCs via up-regulating miR-21 via the activation of AMPK and β-catenin.
    [Abstract] [Full Text] [Related] [New Search]