Open AccessThe downregulation of miR ‐22 and miR ‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K / AKT / GLUT4 pathway
Author(s) -
Li Wei,
Yuan Xianlin,
He Xin,
Yang Li,
Wu Yingyuan,
Deng Xiaofeng,
Zeng Yiwen,
Hu Kesheng,
Tang Bo
Publication year - 2022
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.24557
Subject(s) - glut4 , gestational diabetes , microrna , pi3k/akt/mtor pathway , placenta , downregulation and upregulation , transfection , western blot , protein kinase b , reporter gene , glucose transporter , insulin resistance , biology , endocrinology , chemistry , diabetes mellitus , gene expression , microbiology and biotechnology , gene , insulin , pregnancy , signal transduction , fetus , gestation , genetics
Background Identifying effective regulatory mechanisms will be significant for Gestational diabetes mellitus (GDM) diagnosis and treatment. Methods The expressions of miR‐22 and miR‐372 in placenta tissues from 75 pregnant women with GDM and 75 matched healthy controls and HRT8/SVneo cells (a model of insulin resistance) were analyzed by qPCR. The expressions of PI3K, AKT, IRS, and GLUT4 in high glucose‐treated HRT8/SVneo cells transfected with miR‐22 or miR‐372 mimics or inhibitors was assessed by Western blot. A luciferase gene reporter assay was employed to verify miRNAs' target genes. Results The expressions of miR‐22 and miR‐372 in placental tissues from GDM patients and HRT8/SVneo cells were significantly decreased compared with the respective controls. The GLUT4 expression was significantly decreased in the placenta tissues of GDM and HRT8/SVneo cells with high glucose transfected with miR‐22 and miR‐372 inhibitors. We confirmed that SLC2A4 , the gene encoding GLUT4, was a direct target of miR‐22 and miR‐372. In this study, we report that the lower expressions of miR‐22 and miR‐372 in placental tissue from GDM patients. Conclusion Our results further suggested that the downregulations of miR‐22 and miR‐372 may contribute to GDM through regulating the PI3K/GLUT4 pathway.