LAUSR

OBJECTIVE LncRNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to play an oncogenic role in the occurrence and development of diabetic nephropathy (DN). The aim of our study was to investigate the potential mechanism by which NEAT1 facilitates the progression of DN. PATIENTS AND METHODS Quantitative Real-time polymerase chain reaction (qRT-PCR) was carried out to determine the abundance of NEAT1, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), proliferating cell nuclear antigen (PCNA), Cyclin D1, P38, apoptosis signal-regulating kinase 1 (ASK1), Fibronectin, α smooth muscle actin (α-SMA) and miR-23c in the serum of DN patients, normal patients and mouse mesangial cells (MMCs). Cell proliferation was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), qRT-PCR and Western blot assays. Flow cytometry and Western blot were applied to measure apoptosis of MMCs. Cell fibrosis and epithelial-to-mesenchymal transition (EMT) were analyzed by qRT-PCR and Western blot. The binding sites between miR-23c and NEAT1 were predicted by starBase bioinformatics software, and the relationship was verified by dual-luciferase reporter assay. RESULTS The enrichment of NEAT1 was elevated in the serum of DN patients and MMCs induced by high concentration of glucose. NEAT1 overexpression accelerated proliferation, fibrosis and EMT and restrained apoptosis of MMCs induced by high concentration of glucose. MiR-23c bound to NEAT1, and the inhibition of miR-23c counteracted the suppressive effect of NEAT1 depletion on proliferation, fibrosis and EMT of MMCs induced by high concentration glucose. CONCLUSIONS LncRNA NEAT1 promoted proliferation, fibrosis and EMT while impeded apoptosis of MMCs through sponging miR-23c. LncRNA NEAT1 and miR-23c might be underlying therapeutic targets for the treatment of DN.