miR-765 targeting PDX1 impairs pancreatic β-cell function to induce type 2 diabetes

被引：4

作者：

Zheng, Li ^{[1
]}

Wang, Yalan ^{[1
]}

Li, Yanhong ^{[1
]}

Li, Li ^{[1
]}

Wang, Xiaohong ^{[1
]}

Li, Yan ^{[1
]}

机构：

[1] Wuhan Univ Sci & Technol, Wuhan Wuchang Hosp, Dept Endocrinol, 116 Yangyuan Rd, Wuhan 430063, Peoples R China

来源：

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY | 2023年 / 129卷 / 06期

关键词：

PDX1; miR-765; pancreatic beta-cell; type; 2; diabetes; apoptosis; PROLIFERATION; EXPRESSION; PATHWAY; MASS;

D O I：

10.1080/13813455.2021.1946561

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Type 2 diabetes (T2DM) is a chronic metabolism disorder with a symptom as pancreatic beta-cell dysfunction. In this study, the bioinformatics analysis identified the key regulators (PDX1 and miR-765) in T2DM. By qRT-PCR and western blotting, miR-765 with high expression and PDX1 with low expression were observed in blood samples from T2DM patients and the T2DM cell model. Together with GSIS assay, CCK-8, TUNEL assay, glycolysis assay, and mitochondrial respiration assay, miR-765 overexpression impaired insulin secretion cell viability, glycolysis, and mitochondrial respiration, while enhanced cell apoptosis in pancreatic beta-cell. The Luciferase reporter, RIP, and RNA pull-down assays showed that PDX1 was the target gene of miR-765 in pancreatic beta-cell. Besides, the negative effect of miR-765 on pancreatic beta-cell could be overturned by PDX1 overexpression. In conclusion, we confirmed that miR-765 could cause a detrimental effect on pancreatic beta-cell survival and function by targeting PDX1, which might provide new insight for T2DM therapy.

引用

页码：1279 / 1288

页数：10

共 40 条

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