Abstract
Background : This research aimed to explore the molecular mechanism of LncRNA- plasmacytoma variant translocation 1 (PVT1) in diabetic nephropathy (DN). Methods: Mouse mesangial cells (MMCs) were obtained from diabetic model mice. The real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), Western blot, luciferase reporter gene assay, EdU assay, flow cytometry analysis, AnnexinV-PI double staining, scratch assay, Transwell assay, enzyme-linked immunosorbent assay (ELISA) and luciferase reporter gene assay were performed to reveal the effect of PVT1 on the proliferation, migration, invasion and fibrosis of MMCs cultured in high glucose. Results: PVT1 was overexpressed in both mice kidney tissue and high glucose cultured MMCs. Meanwhile, PVT1 could not only promoted proliferation, migration, invasion and fibrosis of high glucose cultured MMCs, but also regulated the cell cycle from G0/G1 to S phase. Moreover, PVT1 negatively regulated the expression of miR-93-5p in MMCs. Furthermore, the PVT1-miR-93-5p regulatory relation activated the PI3K/Akt/mTOR pathway, which in turn regulated cell proliferation and insulin signaling in high glucose cultured MMCs. Conclusions: PVT1 might promoted proliferation, migration, invasion and fibrosis in high glucose cultured MMCs, which further affected the development of DN. Furthermore, PVT1-miR-93-5p regulatory relation might take part in DN progression via activating the PI3K/Akt/mTOR pathway.