Mechanism of miR-190b with Albumin Nanoparticles as Carrier Mediating Islet β Cells in Gestational Diabetes Mellitus

Author:

Wang Xing1,Lu Yu2,Wang Suyu3,Wang Xueqin1,Yang Shufang2,Zhao Chengyuan2

Affiliation:

1. Department of Endocrinology, Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, Jiangsu, 226001, China

2. Department of Endocrinology, The Affiliated Taizhou People’s Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, 225300, China

3. Department of Endocrinology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, China

Abstract

A variety of diseases are often observed during pregnancy and miR-190b involves in gestational diabetes mellitus (GDM). This study assesses miR-190b’s role in GDM. Electron microscopy analyzed the size of nanoparticles. miR-190b expression in tissues was detected and its effects on islet cells were detected by MTT method, BrdU staining method and ELISA method. Insulin secretion was further detected by molecular biology techniques. Electron microscopy showed similar average particle size of each formulation. miR-190b was overexpressed in the placental tissues of GDM and its overexpression promoted cell proliferation and insulin secretion, whereas downregulation of miR-190b exerted opposite effects. In addition, miR-190b negatively modulated NKX6-1 level and their relationship was confirmed by bioinformatics techniques and a luciferase reporter gene. NKX6-1 overexpression reversed miR-190b mimics’ effect, and miR-190b knockdown promoted insulin secretion by upregulating NKX6-1. The inhibitory effect of miR-190b overexpression on islet β cells using nano-albumin particles as a carrier was partially reversed by NKX6-1 overexpression. Silencing of miR-190b by nano-albumin particles as a carrier promoted β-cell function, which may be one of the mechanisms by which miR-190b affects GDM.

Publisher

American Scientific Publishers

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