scholarly journals Nesfatin-1 alleviates high glucose/high lipid-induced injury of trophoblast cells during gestational diabetes mellitus

Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 12789-12799
Author(s):  
Huanling He ◽  
Yingyu Liu ◽  
Minghe Sun
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Glucose ◽  
Trophoblast Cells ◽  
High Lipid

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

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Chunxia Zhang ◽  
Li Wang ◽  
Jinfeng Chen ◽  
Fei Song ◽  
Yuzhen Guo
Keyword(s):  
Diabetes Mellitus ◽  
Cell Proliferation ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Viability ◽  
High Glucose ◽  
Target Gene ◽  
Trophoblast Cell ◽  
Luciferase Reporter ◽  
Trophoblast Cells

Background. Gestational diabetes mellitus (GDM) seriously affects the health of mothers and infants. The high-glucose-induced inhibition in trophoblast cell viability is an important event in GDM pathogenesis. This study evaluated the expression and clinical significance of miR-136 in GDM patients, and the biological function and related mechanisms of miR-136 in the regulation of trophoblast cell proliferation were explored. Methods. The expression of miR-136 in serum and placenta of GDM patients was measured using quantitative Real-Time PCR. Trophoblast cells were stimulated with high-glucose medium to mimic the pathological changes of GDM, and the effect of miR-136 was examined by CCK-8 assay. A luciferase reporter assay was used to confirm the target gene of miR-136, and the relationship of E2F transcription factor 1 (E2F1) with miR-136 in GDM was further analyzed. Results. miR-136 expression was significantly elevated in GDM serum and tissue samples. By high-glucose treatment, trophoblast cell proliferation was inhibited and miR-136 expression was promoted. The knockdown of miR-136 could promote the proliferation of trophoblast cells exposed to high glucose, whereas the overexpression of miR-136 could suppress it. In addition, E2F1 was identified as a target gene of miR-136, which could mediate the regulatory effect of miR-136 on trophoblast cell proliferation. Conclusion. Collectively, miR-136 expression is increased in both serum and placental tissues in GDM patients, and miR-136 mediates the inhibiting effect of high glucose on trophoblast cell viability by targeting E2F1.

High Glucose Level Induces Cardiovascular Dysplasia During Early Embryo Development

2017 ◽  
Vol 127 (09) ◽  
pp. 590-597
Author(s):  
Yi-mei Jin ◽  
Shu-zhu Zhao ◽  
Zhao-long Zhang ◽  
Yao Chen ◽  
Xin Cheng ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Glucose ◽  
Reactive Oxygen ◽  
Early Embryo ◽  
Yolk Sac ◽  
Oxygen Species ◽  
Excess Reactive Oxygen Species

AbstractThe incidence of gestational diabetes mellitus (GDM) has increased dramatically amongst multiethnic population. However, how gestational diabetes mellitus damages the developing embryo is still unknown. In this study, we used yolk sac membrane (YSM) model to investigate angiogenesis in the developing chick embryo. We determined that in the presence of high glucose, it retarded the growth and extension of the embryonic vascular plexus and it also reduced the density of the vasculature in yolk sac membrane model. Using the same strategy, we used the chorioallantoic membrane (CAM) as a model to investigate the influence of high glucose on the vasculature. We established that high glucose inhibited development of the blood vessel plexus and the blood vessels formed had a narrower diameter than control vessels. Concurrent with the abnormal angiogenesis, we also examined how it impacted cardiogenesis. We determined the myocardium in the right ventricle and left atrium were significantly thicker than the control and also there was a reduction in glycogen content in cardiomyocytes. The high glucose also induced excess reactive oxygen species (ROS) production in the cardiomyocytes. We postulated that it was the excess reactive oxygen species that damaged the cardiomyocytes resulting in cardiac hyperplasia.

High Glucose Suppresses Cardiomyocyte Progenitor Cell Regenerative Capacity and the Role of miR-195/EZH2 Crosstalk in Gestational Diabetes Mellitus

2021 ◽  
Vol 242 ◽  
pp. 162-163
Author(s):  
Pranav Mellacheruvu ◽  
Progyaparamita Saha ◽  
Sameer Ahmad Guru ◽  
Rachana Mishra ◽  
Sudhish Sharma ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Glucose ◽  
Progenitor Cell ◽  
Regenerative Capacity

scholarly journals Mitochondrial dysfunction in placental trophoblast cells experiencing gestational diabetes mellitus

2020 ◽  
Author(s):  
Joshua J. Fisher ◽  
Chelsea L. Vanderpeet ◽  
Lucy A. Bartho ◽  
Daniel R. McKeating ◽  
James S. M. Cuffe ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Mitochondrial Dysfunction ◽  
Trophoblast Cells

scholarly journals Downregulation of miR-451a in plasma may promote prothrombin expression and contribute to high blood coagulation state in gestational diabetes mellitus

2020 ◽  
Vol 19 (10) ◽  
pp. 2079-2084
Author(s):  
Min Qiu ◽  
Zhimin Shangguan ◽  
Hao Zhang
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Blood Coagulation ◽  
High Glucose ◽  
Quantitative Polymerase Chain Reaction ◽  
Hypercoagulable State ◽  
Luciferase Assay ◽  
Keywords Gestational Diabetes ◽  
And Control

Purpose: To investigate F2 and miR-451a levels in gestational diabetes mellitus (GDM) patients, evaluate the potential role of miR-451a in GDM, and to explore its possible downstream targets. Methods: Thromboelastography (TEG) analysis was conducted to analyze coagulation differences between the GDM and control groups. Quantitative polymerase chain reaction (qPCR) and immunoblot were performed to analyze miR-451a and F2 levels after exposure to high glucose and miR-451a mimics or an miR-451a inhibitor. Luciferase assay was used to explore the potential regulatory mechanism. Results: Enhancement of the patients' blood coagulation ability and down-regulated miR-451a expression levels occurred in the plasma of GDM patients. The data further show that hepatocytes exposed to high glucose reduced miR-451a levels and enhanced F2 expression. The  overexpression of miR-451a inhibited the expression of F2. Conclusion: MiR-451a may serve as a promising marker for hypercoagulable state GDM patients Keywords: Gestational diabetes mellitus (GDM), MiR-451a, F2, Hypercoagulable state, Prothrombin, Thromboelastography (TEG)

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