open access

Vol 92, No 8 (2021)
Research paper
Published online: 2021-06-16
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miR-181d promotes pancreatic beta cell dysfunction by targeting IRS2 in gestational diabetes mellitus

Hui Shen12, Jing Sun1, Jing Liu1, Lu Wang1, Lingyun Dong3
·
Pubmed: 34155619
·
Ginekol Pol 2021;92(8):563-570.
Affiliations
  1. Taikang Xianlin Drum Tower Hospital, Nanjing, China
  2. The Affiliated Sir Run Run Hospital of Nanjing Medical University, Nanjing, China
  3. Shanghai Public Health Clinical Center, Shanghai, China

open access

Vol 92, No 8 (2021)
ORIGINAL PAPERS Obstetrics
Published online: 2021-06-16

Abstract

Objectives: Hyperglycemia that develops during pregnancy is a diagnostic criterion of gestational diabetes mellitus (GDM). Current studies have shown that the expression of miRNA-181d is significantly enhanced in the glomeruli of type 2 diabetic. However, the relationship between miR-181d and GDM has never been reported before.
Material and methods: The serum samples were collected from patients with GDM and subjected to qRT-PCR to verify the potential altered the miR-181d expression. In an in vitro GDM model, the miR-181d expression was induced by high glucose treatment, a miR-181d inhibitor was transfected into INS-1 cells to reduce miR-181d expression. Then, the level of insulin mRNA, cell viability, and content of total insulin were analyzed through ELISA, CCK-8 assay, and qRT-PCR assay. The relative apoptosis rates were detected by Annexin-V/PI assays. Finally, the shIRS2 transfection was performed to test whether in pancreatic β cells, IRS2 had similar insulin-enhancing functions as the miR-181d inhibitor.
Results: MiR-181d expression level was positively correlated with fasting blood glucose levels and the inhibition of miR-181d reduced insulin resistance, enhanced cells viability and suppressed high-glucose-induced apoptosis. In addition, the suppression of miR-181d improved the functions of INS-1 cells by targeting IRS2.
Conclusions: In summary, this study indicated that miR-181d modulated the process of insulin signaling and cell viability and apoptosis in pancreatic β cells by targeting IRS-2, suggesting that miR-181d inhibition is a potential target for GDM therapy.

Abstract

Objectives: Hyperglycemia that develops during pregnancy is a diagnostic criterion of gestational diabetes mellitus (GDM). Current studies have shown that the expression of miRNA-181d is significantly enhanced in the glomeruli of type 2 diabetic. However, the relationship between miR-181d and GDM has never been reported before.
Material and methods: The serum samples were collected from patients with GDM and subjected to qRT-PCR to verify the potential altered the miR-181d expression. In an in vitro GDM model, the miR-181d expression was induced by high glucose treatment, a miR-181d inhibitor was transfected into INS-1 cells to reduce miR-181d expression. Then, the level of insulin mRNA, cell viability, and content of total insulin were analyzed through ELISA, CCK-8 assay, and qRT-PCR assay. The relative apoptosis rates were detected by Annexin-V/PI assays. Finally, the shIRS2 transfection was performed to test whether in pancreatic β cells, IRS2 had similar insulin-enhancing functions as the miR-181d inhibitor.
Results: MiR-181d expression level was positively correlated with fasting blood glucose levels and the inhibition of miR-181d reduced insulin resistance, enhanced cells viability and suppressed high-glucose-induced apoptosis. In addition, the suppression of miR-181d improved the functions of INS-1 cells by targeting IRS2.
Conclusions: In summary, this study indicated that miR-181d modulated the process of insulin signaling and cell viability and apoptosis in pancreatic β cells by targeting IRS-2, suggesting that miR-181d inhibition is a potential target for GDM therapy.

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Keywords

gestational diabetes mellitus; miR-181d; pancreatic beta cell; IRS2; insulin resistance

About this article
Title

miR-181d promotes pancreatic beta cell dysfunction by targeting IRS2 in gestational diabetes mellitus

Journal

Ginekologia Polska

Issue

Vol 92, No 8 (2021)

Article type

Research paper

Pages

563-570

Published online

2021-06-16

Page views

1174

Article views/downloads

848

DOI

10.5603/GP.a2021.0077

Pubmed

34155619

Bibliographic record

Ginekol Pol 2021;92(8):563-570.

Keywords

gestational diabetes mellitus
miR-181d
pancreatic beta cell
IRS2
insulin resistance

Authors

Hui Shen
Jing Sun
Jing Liu
Lu Wang
Lingyun Dong

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