MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1

Background Pancreatic beta-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic beta-cell dysfunction. However, the detailed mechanisms remain largely unknown. Methods RT-qPCR, western blotting, and immunofluorescence assays were used to evaluate PRMT1 and miR-574-3p levels. Cell Counting Kit-8, Advanced Dlycation End products (AGEs), Reactive Oxygen Species (ROS), and glucose-stimulated insulin secretion were assayed, and flow cytometry and RT-qPCR were performed to detect the role of PRMT1 and miR-574-3p in MIN6 cells. Luciferase reporter assays were performed to determine the interactions between PRMT1 and miR-574-3p. Results High-glucose treatment resulted in the high expression of PRMT1. PRMT1 silencing could alleviate the reduced proliferation, insulin secretion, and GLUT1 level, in addition to suppressing the induced apoptosis, and AGEs and ROS levels, under high glucose conditions. MiR-574-3p was established as an upstream regulator of PRMT1 using luciferase reporter assays. More importantly, miR-574-3p reversed the effect of PRMT1 silencing in MIN6 cells. Conclusions miR-574-3p suppresses glucose toxicity-induced pancreatic beta-cell dysfunction by targeting PRMT1.

Automated summary

This study found that miR-574-3p suppresses glucose toxicity-induced pancreatic beta-cell dysfunction by targeting PRMT1. The high expression of PRMT1 was associated with reduced proliferation, insulin secretion, and GLUT1 level, as well as increased apoptosis, AGEs, and ROS levels in pancreatic beta cells.