scholarly journals MicroRNA‑1323 serves as a biomarker in gestational diabetes mellitus and aggravates high glucose‑induced inhibition of trophoblast cell viability by suppressing TP53INP1

2021 ◽  
Vol 21 (3) ◽  
Author(s):  
Lijun Liu ◽  
Jun Zhang ◽  
Yujuan Liu
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Viability ◽  
High Glucose ◽  
Trophoblast Cell

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.

scholarly journals Circ-PNPT1 contributes to gestational diabetes mellitus (GDM) by regulating the function of trophoblast cells through miR-889-3p/PAK1 axis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Li Zhang ◽  
Ming Zeng ◽  
Fei Tang ◽  
Jun Chen ◽  
Dongmei Cao ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Viability ◽  
Trophoblast Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Binding Interaction

Abstract Background Gestational diabetes mellitus (GDM) is the most common medical complication of pregnancy. CircRNA polyribonucleotide nucleotidyltransferase 1 (circ-PNPT1) has been found to be abnormally expressed in GDM patients. However, function and mechanism of circ-PNPT1 in GDM remain largely undefined. Methods Levels of circ-PNPT1, microRNA (miR)-889-3p and PAK1 (p21 (RAC1) activated kinase 1) were detected using quantitative real-time polymerase chain reaction and Western blot assays. Cell viability, apoptosis, migration and invasion were determined using cell counting kit-8 assay, flow cytometry, transwell and wound healing assays, respectively. The binding interaction between miR-889-3p and circ-PNPT1 or PAK1 was verified using dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays. Exosomes were obtained from culture media by the use of commercial kits and qualified by transmission electron microscopy (TEM). Results Circ-PNPT1 was highly expressed in the placental tissues of GDM and high glucose (HG)-induced trophoblast cells. Knockdown of circ-PNPT1 reversed HG-induced arrest of trophoblast cell viability, migration, invasion and the promotion of cell apoptosis. Mechanistically, we confirmed circ-PNPT1 could promote the expression of PAK1, the target of miR-889-3p, by directly sponging miR-889-3p, and circ-PNPT1 regulated HG-induced trophoblast cell dysfunction by miR-889-3p/PAK1 axis. Further studies showed circ-PNPT1 was packaged into exosomes and could be internalized by surrounding trophoblast cells. Conclusion Circ-PNPT1 promoted HG-induced trophoblast cell biological dysfunction through miR-889-3p/PAK1 axis. Meanwhile, it could be transferred from HG-induced trophoblast cells to surrounding untreated cells via exosomes.

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.

scholarly journals miR-132 serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell viability

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Xuegui Zhou ◽  
Cuiping Xiang ◽  
Xiaoxia Zheng
Keyword(s):  
Diabetes Mellitus ◽  
Cell Proliferation ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Function ◽  
Fasting Blood Glucose ◽  
Trophoblast Cell ◽  
Operating Characteristics ◽  
Diagnostic Potential

Abstract Background Gestational diabetes mellitus (GDM) leads to poor pregnancy outcomes. Strategies that improve trophoblast cell function are important methods for GDM treatment. This study aimed to investigate the expression and diagnostic potential of microRNA-132 (miR-132) in GDM patients, and further analyzed the effects of miR-132 on HTR-8/SVneo cell proliferation. Methods Quantitative real-time PCR was applied to estimate the expression of miR-132. A receiver operating characteristics curve (ROC) analysis was performed to evaluate the diagnostic value of serum miR-132 in GDM patients. In vitro regulation of miR-132 in trophoblast cell HTR-8/SVneo was achieved by cell transfection, and the effects of miR-132 on cell proliferation were assessed using CCK-8 assay. Results Expression of miR-132 was decreased in serum and placenta tissues in GDM patients compared with the healthy women. A negative correlation was found between the serum miR-132 levels and fasting blood glucose of the GDM patients. A ROC curve shown the serum miR-132 had considerable diagnostic accuracy with an area under the curve (AUC) of 0.898. High glucose (HG) treatment induced an inhibition in HTR-8/SVneo cell proliferation and the expression of miR-132. The overexpression of miR-132 in HTR-8/SVneo cells could markedly rescued the HG - induced suppressed cell proliferation. Conclusion All the data of this study revealed the reduced expression of miR-132 in serum and placenta tissues of GDM, and serum miR-132 serves a candidate biomarker in the diagnosis of GDM. miR-132 may act a protective role against GDM via enhancing the trophoblast cell proliferation.

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 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)

Sign in / Sign up

Export Citation Format

Share Document