Downregulation of lncRNA NEAT1 inhibits mouse mesangial cell proliferation, fibrosis, and inflammation but promotes apoptosis in diabetic nephropathy.

This study aimed to investigate the effect of long non-coding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on mouse mesangial cells (MMCs) proliferation, apoptosis, fibrosis as well as inflammation in diabetic nephropathy (DN). MMCs (SV40 MES13 cells) were cultured under 30 mM glucose to construct DN cellular model (high glucose (HG) group); meanwhile, MMCs cultured under 5.6 mM glucose (normal glucose (NG) group) and 5.6 mM glucose plus 24.4 mM 3-O-methyl-D-glucose (osmotic control (OC) group) served as controls, and lnc-NEAT1 expression was determined by qPCR assay. Lnc-NEAT1 interference plasmids and control interference plasmids were transfected into DN cellular model as Sh-NEAT1 group and Sh-NC group. Cell proliferation, apoptosis, fibrosis, and inflammation were detected using Counting Kit-8, Annexin V/propidium iodide, western blot and quantitative polymerase chain reaction assays. Lnc-NEAT1 expression was elevated in HG group compared to NG group and OC group. Cell proliferation was decreased, and proliferative marker protein Cyclin D1 and proliferating cell nuclear antigen expressions also decreased in Sh-NEAT1 group compared to Sh-NC group. For cell apoptosis, apoptosis rate was increased, and apoptotic protein Cleaved Caspase3 expression enhanced but anti-apoptosis protein Bcl-2 expression decreased in Sh-NEAT1 group compared to Sh-NC group. For fibrosis markers (including fibronectin and collagen I) and inflammatory cytokines (including tumor necrosis factor-α, interleukin-1β and interleukin-6), their expressions were reduced in Sh-NEAT1 group compared to Sh-NC group. Lnc-NEAT1 is overexpressed, and its downregulation inhibits cell proliferation, fibrosis, and inflammation but promotes cell apoptosis in HG-induced MMCs DN cellular model. IJCEP