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Published on: January 23, 2018
MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1
Lixia Lv1, Xiumin Wang2, Jinhua Shen3
1Department of Endocrinology and Metabolism, Chengdu First People's Hospital, HI-TECH Zone, 18 Wanxiang North Road, Chengdu, 610041, Sichuan, China. lixialv87@163.com.
Background:
Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-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 β-cell dysfunction by targeting PRMT1.
Insights
MicroRNA-574-3p (miR-574-3p) combats pancreatic beta-cell dysfunction in type 2 diabetes by targeting Protein Arginine Methyltransferase 1 (PRMT1). This finding offers new insights into diabetes mechanisms.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Pancreatic beta-cell dysfunction is a hallmark of type 2 diabetes mellitus.
- Protein Arginine Methyltransferase 1 (PRMT1) is implicated in beta-cell dysfunction, but its precise role is unclear.
Purpose of the Study:
- To investigate the role of PRMT1 and miR-574-3p in high glucose-induced pancreatic beta-cell dysfunction.
- To elucidate the regulatory relationship between PRMT1 and miR-574-3p.
Main Methods:
- Quantitative real-time PCR (RT-qPCR), western blotting, and immunofluorescence assays.
- Cell viability assays (Cell Counting Kit-8), measurement of Advanced Glycation End products (AGEs) and Reactive Oxygen Species (ROS), and glucose-stimulated insulin secretion assays.
- Luciferase reporter assays to confirm direct interaction between miR-574-3p and PRMT1.
Main Results:
- High glucose conditions increased PRMT1 expression in MIN6 cells.
- PRMT1 silencing ameliorated high glucose-induced beta-cell dysfunction, including improved proliferation, insulin secretion, GLUT1 levels, and reduced apoptosis, AGEs, and ROS.
- MiR-574-3p was identified as a direct upstream regulator of PRMT1 and could reverse the effects of PRMT1 silencing.
Conclusions:
- miR-574-3p plays a protective role against glucose toxicity-induced pancreatic beta-cell dysfunction.
- Targeting PRMT1 by miR-574-3p is a key mechanism underlying this protective effect.
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