Differential Expression of miR-136 in Gestational Diabetes Mellitus Mediates the High-Glucose-Induced Trophoblast Cell Injury through Targeting E2F1

Zhang, Chunxia; Wang, Li; Chen, Jinfeng; Song, Fei; Guo, Yuzhen

doi:10.1155/2020/3645371

Cited by 17 publications

(6 citation statements)

References 41 publications

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“…17 This study found that the viability of trophoblast cells cultured in high glucose in vitro decreased. The results are consistent with the study by Zhang et al 18 High-glucose-induced reduction in viability of trophoblast cells is involved in the pathogenesis of GDM. However, in clinical practice, the majority of GDM patients exhibit excessive placental tissue growth and give birth to macrosomic infants.…”

Section: Discussionsupporting

confidence: 93%

High glucose regulates the cells dysfunction of human trophoblast HTR8/SVneo cells by downregulating GABRP expression

Wang,

Qiu

2024

Adv Clin Exp Med

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Background.In response to the high-glucose environment in patients with gestational diabetes mellitus (GDM), trophoblast cells undergo a series of pathological changes. Gamma-aminobutyric acid type A receptor subunit pi (GABRP) is involved in the development of pregnancy-related diseases and regulation of blood glucose.Objectives. To explore the relationship between GABRP and hyperglycemia stimulation in GDM patients, and to provide preliminary experimental evidence for whether GABRP has the potential as a molecular target for the treatment of GDM. Materials and methods.Within 30 min after birth, placental samples were taken from 20 GDM patients and 20 pregnant women without GDM. Human chorionic trophoblast HTR-8/SVneo cells were utilized for in vitro experimental investigation. We explored changes in GABRP expression in placental samples and HTR-8/ Svneo cells using western blot and quantitative reverse transcription polymerase chain reaction (RT-qPCR). Cells in the high-glucose treatment group were exposed to medium containing 25 mM glucose. To explore the relationship between GABRP and high-glucose stimulation, GABRP was overexpressed in HTR-8/SVneo cells. We monitored the cell viability, invasion and migration abilities using Cell Counting Kit-8 (CCK-8), transwell and scratch assays, respectively.Results. We found that GABRP expression was significantly reduced in placental samples from GDM patients. Furthermore, high-glucose treatment decreased the expression level of GABRP in HTR-8/SVneo cells. High-glucose stimulation reduced the cell viability, invasion and migration abilities. GABRP overexpression reversed the biological dysfunction of the cells induced by high-glucose stimulation.Conclusions. Hyperglycemia in GDM patients downregulates the expression of GABRP, and overexpression of GABRP promotes the viability, migration and invasive ability of HTR8-/SVneo cells.

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Section: Discussionsupporting

confidence: 93%

High glucose regulates the cells dysfunction of human trophoblast HTR8/SVneo cells by downregulating GABRP expression

Wang,

Qiu

2024

Adv Clin Exp Med

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“…HG-induced surrounding around trophoblast cells aggravated the injury of cells, influenced cell viability, and further aroused dysfunction of cells (25). Multitudinous researches state the function of lncRNAs on trophoblast cell functions.…”

Section: Discussionmentioning

confidence: 99%

LncRNA XIST serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell via miR-497-5p/FOXO1 axis

Yuan

Shi

et al. 2021

Cardiovasc Diagn Ther

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Background: Gestational diabetes mellitus (GDM) is increasingly common in pregnancy. This study's purpose was to identify the expression of XIST and manifest the potential mechanism of XIST in GDM.Methods: Ninety-three patients with GDM and 93 normal pregnant women were included in this investigation. qRT-PCR was conducted to evaluate the expression of miR-497-5p and XIST and the relationship between XIST and fasting blood glucose (FBG) was explored by Pearson assay. The clinical diagnosis of XIST on GDM patients was validated by the receiver operator characteristic (ROC) curve. Cell counting kit-8 (CCK-8) was applied to elucidate cell viability. Luciferase reporter assay was performed to document the relationship among XIST, miR-497-5p, and FOXO1.Results: The expression of XIST was increased in GDM patients and HTR-8/SVneo cell models caused by high glucose (HG). The expression of XIST was associated with the FBG levels and appeared to be a feasible indicator in discriminating GDM patients. The expression of miR-497-5p was prominently reduced in GDM patients and cell models. Inhibition of XIST might alleviate the adverse function of HG on cell viability via sponging miR-497-5p. FOXO1 was proved to be a downstream target gene of miR-497-5p.Conclusions: Overexpression of XIST and downregulation of miR-497-5p were indicated in this publication. XIST might serve as a promising diagnostic marker for GDM patients. XIST/miR-497-5p/ FOXO1 axis played a critical role in the regulation of trophoblast cells.

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“…Expression of the CCND1 gene plays a role in the development of obesity [189], but this gene might be associated with progression of GDM. FOXO1 [190], hsa-mir-1207-5p [191], hsa-mir-4651 [191], hsa-mir-222-3p [192] and E2F1 [193] are essential for the progression of GDM.…”

Section: Discussionmentioning

confidence: 99%

Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus

Vastrad¹,

Vastrad²,

Tengli

2021

Preprint

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Gestational diabetes mellitus (GDM) is one of the metabolic diseases during pregnancy. The identification of the central molecular mechanisms liable for the disease pathogenesis might lead to the advancement of new therapeutic options. The current investigation aimed to identify central differentially expressed genes (DEGs) in GDM. The transcription profiling by array data (E-MTAB-6418) was obtained from the ArrayExpress database. The DEGs between GDM samples and non GDM samples were analyzed with limma package. Gene ontology (GO) and REACTOME enrichment analysis were performed using ToppGene. Then we constructed the protein-protein interaction (PPI) network of DEGs by the Search Tool for the Retrieval of Interacting Genes database (STRING) and module analysis was performed. Subsequently, we constructed the miRNA-hub gene network and TF-hub gene regulatory network by the miRNet database and NetworkAnalyst database. The validation of hub genes was performed through receiver operating characteristic curve (ROC). Finally, the candidate small molecules as potential drugs to treat GDM were predicted by using molecular docking. Through transcription profiling by array data, a total of 869 DEGs were detected including 439 up regulated and 430 down regulated genes. Biological process analysis of GO enrichment analysis showed these DEGs were mainly enriched in reproduction, nuclear outer membrane-endoplasmic reticulum membrane network, identical protein binding, cell adhesion, supramolecular complex and signaling receptor binding. Signaling pathway enrichment analysis indicated that these DEGs played a vital in cell surface interactions at the vascular wall and extracellular matrix organization. Ten genes, HSP90AA1, EGFR, RPS13, RBX1, PAK1, FYN, ABL1, SMAD3, STAT3, and PRKCA in the center of the PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network were associated with GDM, according to ROC analysis. Finally, the most significant small molecules were predicted based on molecular docking. Our results indicated that HSP90AA1, EGFR, RPS13, RBX1, PAK1, FYN, ABL1, SMAD3, STAT3, and PRKCA could be the potential novel biomarkers for GDM diagnosis, prognosis and the promising therapeutic targets. The current might be essential to understanding the molecular mechanism of GDM initiation and development.

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Differential Expression of miR-136 in Gestational Diabetes Mellitus Mediates the High-Glucose-Induced Trophoblast Cell Injury through Targeting E2F1

Cited by 17 publications

References 41 publications

High glucose regulates the cells dysfunction of human trophoblast HTR8/SVneo cells by downregulating GABRP expression

High glucose regulates the cells dysfunction of human trophoblast HTR8/SVneo cells by downregulating GABRP expression

LncRNA XIST serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell via miR-497-5p/FOXO1 axis

Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus

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