Background: LncRNA-ATB is a long noncoding RNAs (lncRNA) activated by transforming growth factor β (TGF-β) and it has important biological functions in tumours and nontumor diseases. Meanwhile, TGF-β is the most critical regulatory factor in the process of nephrotic fibrosis and calcium oxalate (CaOx) crystal-induced renal injury. The present study aimed to investigate the biological function and mechanism of lncRNA-ATB in CaOx crystal-induced renal injury.
Methods: The expression level of lncRNA-ATB was detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), the expression levels of epithelial-mesenchymal transition (EMT) markers and TGF-β1 were detected by qRT-PCR and western bloting, cell proliferation was measured with the CCK-8 kit, cell apoptosis was measured by flow cytometry, and cell injury was detected with the Cytotoxicity lactate dehydrogenase (LDH) Assay kit.
Results: The expression levels of lncRNA-ATB and TGF-β1 significantly increased in HK-2 cells after coincubation with calcium oxalate monohydrate (COM). COM stimulation caused significant injury in HK-2 cells, induced cell apoptosis, inhibited cell proliferation, and induced EMT changes . After COM stimulation, the expression levels of epithelial cell markers E-cadherin and zonula occludens (ZO)-1 in HK-2 cells significantly decreased, whereas the levels of mesenchymal cell markers N-cadherin and vimentin significantly increased. Interference with lncRNA-ATB expression significantly relieved COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT changes. The expression levels of the microRNA-200 (miR-200) family in HK-2 cells after coincubation with COM significantly decreased. MiR-200a mimics relieved the COM-induced cell injury, apoptosis, proliferation inhibition, and EMT changes, whereas miR-200a inhibitors abolished the lncRNA-ATB interference-induced relief of COM-induced cell injury, apoptosis, proliferation inhibition, and EMT.
Conclusion: lncRNA-ATB promote d COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT to participate in the process of CaOx crystal-induced renal injury by sponging miR-200s.