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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 Shen, Jing Sun, Jing Liu, Lu Wang, Lingyun Dong
DOI: 10.5603/GP.a2021.0077
·
Pubmed: 34155619

open access

Ahead of Print
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

Ahead of Print

Article type

Research paper

Published online

2021-06-16

DOI

10.5603/GP.a2021.0077

Pubmed

34155619

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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