scholarly journals miR-520h inhibits cell survival by targeting mTOR in gestational diabetes mellitus

2021 ◽  
Author(s):  
Jie Wen ◽  
Xiaoxia Bai
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Target Gene ◽  
Cell Model ◽  
Fasting Blood Glucose ◽  
Luciferase Reporter ◽  
Maternal Glucose

Gestational diabetes mellitus (GDM) is a type of diabetes that occurs during pregnancy due to abnormal maternal glucose metabolism. This study aimed to investigate the effect of miR-520h and its potential target gene on the progression of GDM. The blood samples were taken from healthy pregnant women and GDM patients. Human villous trophoblasts HTR-8/SVNEO cells were treated with 25 mM glucose and were considered as the GDM cell model. The miR-520h level was detected using qRT-PCR in the serum and GDM cell model. The correlation analysis between fasting blood-glucose (FBG) level and miR-520h expression was analyzed. The target relationship between miR-520h and mTOR was verified using dual luciferase reporter assay. HG-induced cells were transfected with miR-520h mimic or miR-520h inhibitor and pCDNA3-mTOR vector or their NCs. Cell viability, apoptosis and mTOR expression level were detected using CCK-8, flow cytometry and western blotting, respectively. The results showed that the miR-520h serum level was up-regulated in the GDM patients’ serum and GDM cell model, and was positively correlated with FBG of GDM patients. High glucose (HG) inhibited HTR-8/SVNEO cell viability and decreased mTOR expression, while it promoted apoptosis. Then, the effects of HG on HTR-8/SVNEO cells were reversed by miR-520h inhibitor. Moreover, mTOR was identified as a target gene downstream of miR-520h. The overexpression of mTOR alleviated miR-520h mimic-induced reduction in cell viability and enhancement in cell apoptosis in the GDM cell model. In conclusion, miR-520h could inhibit cell viability and promote cell apoptosis by regulating mTOR expression in the GDM cell model. Hence, miR-520h might be a potential and important marker for the diagnosis and treatment of GDM.

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.

scholarly journals miR-377 inhibition enhances the survival of trophoblast cells via upregulation of FNDC5 in gestational diabetes mellitus

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 464-471
Author(s):  
Zhaozhao Hua ◽  
Dana Li ◽  
Anqin Wu ◽  
Ting Cao ◽  
Shi Luo
Keyword(s):  
Diabetes Mellitus ◽  
Cell Growth ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cell Apoptosis ◽  
Fasting Blood Glucose ◽  
Luciferase Assay ◽  
Cell Vitality ◽  
Fibronectin Type Iii ◽  
Fibronectin Type Iii Domain

Abstract Gestational diabetes mellitus (GDM) is a metabolic dysregulation closely related to both obesity and type 2 diabetes; however, the molecular mechanism underlying GDM is still unclear. The purpose of this study was to investigate the effects of microRNA-377 (miR-377-3p) and fibronectin type III domain containing 5 (FNDC5) in regulating the cell growth of trophoblasts under high glucose (HG) conditions during the development of GDM. Serum miR-377-3p was upregulated and positively correlated with fasting blood glucose level in GDM patients. miR-377-3p downregulation increased the cell vitality and suppressed the cell apoptosis of HG-treated HTR-8/SVneo and BeWo cells. Using TargetScan prediction, luciferase assay, and western blot, it was found that miR-377-3p could target FNDC5 and suppress its expression. However, FNDC5 downregulation abolished the effect of miR-377-3p inhibitor in HTR-8/SVneo cells. Together, miR-377 is a potential target for GDM biomarker, which promotes cell growth and suppresses cell apoptosis, partly through the upregulation of FNDC5.

scholarly journals Association between maternal glucose levels during pregnancy and gestational diabetes mellitus: an analytical cross-sectional study

2015 ◽  
Vol 7 (1) ◽  
Author(s):  
Gisele Seabra ◽  
Cláudia Saunders ◽  
Patrícia de Carvalho Padilha ◽  
Lenita Zajdenverg ◽  
Letícia Barbosa Gabriel da Silva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Glucose Levels ◽  
Maternal Glucose Levels ◽  
Maternal Glucose

scholarly journals GESTATIONAL DIABETES MELLITUS

2012 ◽  
Vol 19 (04) ◽  
pp. 462-468
Author(s):  
M. IKRAM ◽  
SYED HAIDER HASAN ALAM ◽  
SHAFQAT MUKHTAR ◽  
M. Saeed
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Gestational Diabetes Mellitus ◽  
Glucose Tolerance Test ◽  
Fasting Blood Glucose ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Introduction: Gestational diabetes mellitus is common disorder in pregnancy. It is associated with adverse pregnancy outcome. There is no consensus regarding the optimal approach to screening of gestational diabetes mellitus. The present study has tried toobserve the value of fasting blood glucose in screening of gestational diabetes. Objective: To determine the frequency of patients in whomfasting blood glucose and 100gm glucose tolerance show agreement for screening of gestational diabetes mellitus at 24 -28 wks. Studydesign: Comparative cross sectional study. Settings: The study was conducted at Gynecology and Obstetrics department Shaikh ZayedFederal Post Graduate Institute Lahore. Duration of study with dates: 6 months from 12Nov 2010 to 11 May 2011. Material and method: Thestudy included 135 booked patients with positive family history of diabetes mellitus. All patients underwent fasting blood glucose at 24-28 weeksof gestation, regardless of results of fasting blood glucose on next visit they underwent 100g oral glucose tolerance test (OGTT). The agreementbetween fasting blood glucose and 100g oral glucose tolerance test was calculated in frequency and percentages. Results: The mean age ofwomen in studied population was 27.15±3.70.Out of 135 patients 86.7 %( 117) showed agreement between results of fasting blood glucose and100g OGTT while 13.31 %( 18) showed no agreement between both of the tests. Conclusions: Fasting blood glucose is a good screeningoption for gestational diabetes mellitus along with positive history. It provides a simple, cheap and more practical test for screening of gestationaldiabetes mellitus. However diagnostic confirmation with 100g OGTT should be done.

scholarly journals miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Pingping Wang ◽  
Zengfang Wang ◽  
Guojie Liu ◽  
Chengwen Jin ◽  
Quan Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Macrophage Polarization ◽  
Vital Role ◽  
Luciferase Reporter ◽  
M2 Macrophage ◽  
And Migration

MicroRNA (miRNA) has been widely suggested to play a vital role of in the pathogenesis of gestational diabetes mellitus (GDM). We have previously demonstrated that miR-657 can regulate macrophage inflammatory response in GDM. However, the role of miR-657 on M1/M2 macrophage polarization in GDM pathogenesis is not clear yet. This study is aimed at elucidating this issue and identifying novel potential GDM therapeutic targets based on miRNA network. miR-657 is found to be upregulated in placental macrophages demonstrated by real-time PCR, which can enhance macrophage proliferation and migration in vitro. Luciferase reporter assay shows the evidence that FAM46C is a target of miR-657. In addition, miR-657 can promote macrophage polarization toward the M1 phenotype by downregulating FAM46C in macrophages. The present study strongly suggests miR-657 is involved in GDM pathogenesis by regulating macrophage proliferation, migration, and polarization via targeting FAM46C. miR-657/FAM46C may serve as promising targets for GDM diagnosis and treatment.

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.

scholarly journals Expression of IRS1 Gene in Pregnant Women with Gestational Diabetes Mellitus, in The Third Trimester

2021 ◽  
pp. 787-792
Author(s):  
Zainab k. Hussain ◽  
Jabbar H. Yenzeel ◽  
Hayfa H. Hassani
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Lipid Profile ◽  
Fasting Blood Glucose ◽  
Rna Extraction ◽  
Third Trimester ◽  
Healthy Women ◽  
And Control

To study the genetic effect of gestational diabetes mellitus by study IRS1gene expression in female with Gestational diabetes mellitus. It is characterized high level of blood glucose, especially during first trimester then increased during the 2nd and 3rd trimester of the pregnancy period. The blood samples taken from one hundred twenty healthy women and female with gestational diabetes mellitus in 3rd trimester period of pregnancy, level of fasting blood glucose (FBG) also HbA1c% measured to diagnose GDM, in addition to lipid profile (cholesterol, triglyceride, HDL, LDL, and VLDL), molecular study consist of RNA extraction and qRT- PCR for IRS1gene expression determination. The fasting blood glucose mg/dl and HbA1c% level was increased highly significantly (P<0.01) between patients and control (healthy women) in 3rd trimester stage in addition lipid profile included )serum cholesterol, serum triglyceride, LDL and VLDL( (mg/dl) but level of HDL (mg/dl) was decreased highly significantly (P<0.01) between patients and control. The result showed high significant of IRS1 expression gene in control (1.00 ± 0.00) while in patients (0.147 ± 0.02). The low expression of IRS1 gene was connected with gestational diabetes mellitus comparison in control (healthy women) in Iraqi female in third trimester of pregnancy

Sign in / Sign up

Export Citation Format

Share Document