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  • Title: Abnormal expression of TRIAP1 and its role in gestational diabetes mellitus-related pancreatic β cells.
    Author: Li L, Yang K, Ye F, Xu Y, Cao L, Sheng J.
    Journal: Exp Ther Med; 2021 Mar; 21(3):187. PubMed ID: 33488796.
    Abstract:
    Gestational diabetes mellitus (GDM) is a disease that is typically characterized by insulin resistance and pancreatic β cell dysfunction. Currently, the role of TP53-regulated inhibitor of apoptosis 1 (TRIAP1) in the process of GDM remains to be elucidated. Therefore, the present study investigated the effects of TRIAP1 on GDM-related pancreatic β cells. Reverse transcription-quantitative PCR and western blot assays were conducted to analyze the expression levels of TRIAP1 in the peripheral blood of patients with GDM and subjects with healthy pregnancies. Subsequently, TRIAP1 small interfering RNA (siRNA), control siRNA, TRIAP1 plasmid and control plasmid were transfected into INS-1 cells to assess the effects of TRIAP1 on pancreatic β cells. ELISA was used to assess the total insulin content and insulin secretion of pancreatic β cells. MTT and flow cytometry assays were performed to determine the viability and apoptosis of pancreatic β cells. The results demonstrated that TRIAP1 expression was downregulated in peripheral blood samples from patients with GDM. Transfection with TRIAP1 siRNA significantly decreased the levels of total insulin content and reduced insulin secretion in pancreatic β cells. In addition, downregulation of TRIAP1 in pancreatic β cells significantly induced cell apoptosis and reduced cell viability. Accordingly, transfection of INS1 cells with TRIAP1 siRNA increased the levels of the apoptosis-associated genes apoptotic protease-activating factor 1, caspase-3, caspase-7 and caspase-9. However, transfection of the cells with TRIAP1 plasmid resulted in the opposite effects. TRIAP1 increased the growth of pancreatic β cells and their ability to secrete insulin, thus playing a protective role in GDM. The findings verified the effects and the underlying mechanism of TRIAP1 in pancreatic β cells and may provide additional clinical applications for the therapy of GDM.
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