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The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway
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 mode...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279990/ https://www.ncbi.nlm.nih.gov/pubmed/35712865 http://dx.doi.org/10.1002/jcla.24557 |
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author | Li, Wei Yuan, Xianlin He, Xin Yang, Li Wu, Yingyuan Deng, Xiaofeng Zeng, Yiwen Hu, Kesheng Tang, Bo |
author_facet | Li, Wei Yuan, Xianlin He, Xin Yang, Li Wu, Yingyuan Deng, Xiaofeng Zeng, Yiwen Hu, Kesheng Tang, Bo |
author_sort | Li, Wei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9279990 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92799902022-07-15 The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway Li, Wei Yuan, Xianlin He, Xin Yang, Li Wu, Yingyuan Deng, Xiaofeng Zeng, Yiwen Hu, Kesheng Tang, Bo J Clin Lab Anal Research Articles 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. John Wiley and Sons Inc. 2022-06-17 /pmc/articles/PMC9279990/ /pubmed/35712865 http://dx.doi.org/10.1002/jcla.24557 Text en © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Articles Li, Wei Yuan, Xianlin He, Xin Yang, Li Wu, Yingyuan Deng, Xiaofeng Zeng, Yiwen Hu, Kesheng Tang, Bo The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title | The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title_full | The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title_fullStr | The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title_full_unstemmed | The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title_short | The downregulation of miR‐22 and miR‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the PI3K/AKT/GLUT4 pathway |
title_sort | downregulation of mir‐22 and mir‐372 may contribute to gestational diabetes mellitus through regulating glucose metabolism via the pi3k/akt/glut4 pathway |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279990/ https://www.ncbi.nlm.nih.gov/pubmed/35712865 http://dx.doi.org/10.1002/jcla.24557 |
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