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.
Highlights
Cataract is the loss of normal transparency of the crystalline lens, which can reduce light transmission to the retina, resulting in decreased visual acuity and functional disability [1, 2]
We constructed oxidative stress model of human lens epithelial cells (HLECs) and found Long non-coding RNAs (lncRNAs) Antisense non-coding RNA in the INK4 locus (ANRIL) could attenuate H2O2-induced cell injury. miR-21 expression was positively regulated by lncRNA ANRIL expression, and miR-21 inhibition could reverse the effects of lncRNA ANRIL on HLECs under stimulation of H2O2
Phosphorylation of AMPK and expression of β-catenin were increased by lncRNA ANRIL, possibly through up-regulating miR-21
Summary
Cataract is the loss of normal transparency of the crystalline lens, which can reduce light transmission to the retina, resulting in decreased visual acuity and functional disability [1, 2]. As a leading cause of blindness, cataract accounts for approximately half of the cases of blindness worldwide [3]. The number of people suffered cataract in the United States is going to reach 50 million by the 2050 due to the increase of life expectancy [4]. Several risk factors such as diarrhea, aging, sunlight, smoking, diabetes, malnutrition, hypertension and renal failure have been identified for cataract formation [5, 6]. Previous studies have proved that the apoptosis of lens epithelial cells is a common cellular basis for the formation of non-congenital cataract in human and mammalians [7, 8]. Proliferation and apoptosis of lens epithelial cells are of great importance for development of cataract
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