scholarly journals Suppression of PNPase Alleviates Gestational Diabetes Mellitus-cardiovascular Injury through Up-regulating MicroRNA-26a and Down-regulating PTEN

2021 ◽  
Author(s):  
Li Liu ◽  
Haiying Wu# ◽  
Xianghong Cheng
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Saturated Fat ◽  
Scratch Test ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
And Migration

Abstract Objective: Gestational diabetes mellitus (GDM) is often accompanied by cardiovascular injury (CI), while the specific pathology remains largely unknown. The purpose of this study was to investigate the role of Polynucleotide Phosphorylase (PNPase) in GDM-CI.Methods: GDM-CI rats were modeled by giving high-glucose and high-saturated fat compound feed, and PNPase and miR-26a expression in rats was determined. Vascular smooth muscle cells (VSMCs) were isolated, and cells were transfected with si-PNPase, miR-26a mimic, or si-PNPase + miR-26a inhibitor. Cell proliferation, apoptosis and migration of VSMCs were measured by CCK-8 assay, flow cytometry, and scratch test. Dual-luciferase reporter gene assay was performed to verify the targeting relationship between miR-26a and PTEN. RT-qPCR was implemented to detect the expression levels of miR-26a and PTEN among cells in each group.Results: GDM-CI increased PNPase expression and decreased miR-26a expression in cardiovascular tissues of GDM-CI rats. Silencing PNPase and miR-26a upregulation reduced VSMC apoptosis, and enhanced proliferation and migration abilities in GDM-CI. Treatment with miR-26a inhibitor reversed the alleviating effect of inhibiting PNPase expression on GDM-CI. There was a targeting relationship between miR-26a and PTEN, and miR-26a mimic inhibited the expression of PTEN. Suppressed PTEN was found to relieve the GDM-CI.Conclusion: This study suggests that suppression of PNPase alleviates GDM-CI through up-regulating miR-26a and down-regulating PTEN.

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-495-3p Depresses Cell Proliferation and Migration By Down-Regulating HMGB1 in Colorectal Cancer

2021 ◽  
Author(s):  
Zhang Jieling ◽  
Li Kai ◽  
Zheng Huifen ◽  
Zhu Yiping
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
And Migration ◽  
Cancer Tissues

Abstract Background: MicroRNAs play an important role in the genesis and progression of tumors, including colorectal cancer (CRC), which has a high morbidity and mortality rate. In this research, the role of miR-495-3p and HMGB1 in CRC was investigated.Methods: We performed qRT-PCR to detect the expression of miR-495-3p in colorectal cancer tissues and cell lines. Functional experiments such as CCK-8 assay, EDU assay, Transwell assay and apoptosis assay were conducted to explore the effects of miR-495-3p on the proliferation, migration and apoptosis of CRC cells in vitro. Then, the use of database prediction, dual-luciferase reporter gene assay and functional experiments verified the role of miR-495-3p target gene HMGB1 in CRC. Finally, rescue experiments was performed to investigate whether overexpression of HMGB1 could reverse the inhibitory effect of miR-495-3p on CRC cell proliferation in vivo and in vitro.Results: miR-495-3p was down-regulated in colorectal cancer tissues and cell lines, and could inhibit the proliferation and migration of colorectal cancer cells, and promote cell apoptosis. The database prediction and dual-luciferase reporter gene assay showed that HMGB1 was the downstream target gene of miR-495-3p. We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo.Conclusion: Our research shows that miR-495-3p inhibits the progression of colorectal cancer by down-regulating the expression of HMGB1, which indicates that miR-495-3p may become a potential therapeutic target for colorectal cancer.

scholarly journals miR-519d downregulates LEP expression to inhibit preeclampsia development

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1215-1227
Author(s):  
Hairui Cai ◽  
Dongmei Li ◽  
Jun Wu ◽  
Chunbo Shi
Keyword(s):  
Scratch Test ◽  
Underlying Mechanism ◽  
Normal Pregnancy ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Transwell Invasion Assay ◽  
Gene Assay ◽  
Invasive Capacity

Abstract The purpose of the current study was to characterize role of microRNA (miR)-519d in trophoblast cells and preeclampsia (PE) development and its potential underlying mechanism. Regulation of leptin (LEP) by miR-519d was verified using a dual-luciferase reporter gene assay. Loss- and gain-of-function assays were conducted to detect the roles of miR-519d and LEP in proliferation, migratory ability, and invasive capacity of HTR-8/SVneo cells by means of CCK-8 assay, scratch test, and Transwell invasion assay, respectively. The cell apoptosis rate and cycle distribution were analyzed by flow cytometry. LEP expression was elevated, whereas miR-519d level was suppressed in the PE placenta samples compared with those from normal pregnancy. Depletion of LEP promoted proliferation, migratory ability, and invasive capacity and repressed apoptosis. miR-519d could bind 3′ untranslated regions (3′UTRs) of LEP, the extent of which correlated negatively with LEP expression. miR-519d suppressed the expression of LEP in HTR-8/SVneo cells. Moreover, overexpression of miR-519d promoted survival and migratory ability of HTR-8/SVneo cells. Taken together, we find that miR-519d targeted LEP and downregulated its expression, which could likely inhibit the development of PE.

scholarly journals MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes Mellitus

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Pingping Wang ◽  
Zhenzhi Ma ◽  
Zengyan Wang ◽  
Ximei Wang ◽  
Guifeng Zhao ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Macrophage Polarization ◽  
Luciferase Reporter ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
M2 Macrophage Polarization

The role of microRNA (miRNA) in gestational diabetes mellitus has been widely investigated during the last decade. However, the altering effect of miR-6869-5p on immunity and placental microenvironment in gestational diabetes mellitus is largely unknown. In our study, the expression of miR-6869-5p was documented to be significantly decreased in placenta-derived mononuclear macrophages, which was also negatively related to PTPRO. Besides, PTPRO was negatively regulated by miR-6869-5p in placenta-derived mononuclear macrophages. In vitro, miR-6869-5p inhibited macrophage proliferation demonstrated by EdU and CCK-8 experiments. The inflammatory response in macrophages was also significantly inhibited by miR-6869-5p, which could regulate PTPRO as a target documented by luciferase reporter assay. Moreover, miR-6869-5p promoted M2 macrophage polarization and thus restrain inflammation. Accordingly, miR-6869-5p is involved in maintaining placental microenvironment balance by preventing from inflammation and inducing M2 macrophages in gestational diabetes mellitus.

scholarly journals The role of circular RNA circ_0008285 in gestational diabetes mellitus by regulating the biological functions of trophoblasts

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Haitian Chen ◽  
Shaofeng Zhang ◽  
Yanxin Wu ◽  
Zhuyu Li ◽  
Dongyu Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Throughput Sequencing ◽  
Expression Profiles ◽  
Circular Rna ◽  
Circular Rnas ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Circular RNAs (circRNAs) has emerged as vital regulator involved in various diseases. In this study, we identified and investigated the potential circRNAs involved in gestational diabetes mellitus (GDM). Methods High-throughput sequencing was used to collect the plasma circRNAs expression profiles of GDM patients. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) was used to measure the expressions of circ_0008285 and circ_0001173 in the plasma specimens. The Pearson’s correlation test was employed to assess the correlation between 2 circRNAs expression and the clinicopathologic data. Two circRNAs expression was verified in high glucose (HG)-induced HTR-8/SVneo cells. MTS, transwell assay was used to evaluate the effects of circ_0008285 expression on HG-induced HTR-8/SVneo cells. The network of circ_0008285 was constructed using cytocape. Results In GDM patients, the expression of circ_0008285 was significantly upregulated, while that of circ_0001173 was decreased. Circ_0008285 was significantly correlated with the total cholesterol and LDL-C levels. Circ_0001173 was significantly correlated with glycated hemoglobin. HG promoted the proliferation, invasion, and migration in HTR-8/SVneo cells, while the knockdown of circ_0008285 exerted reverse effects. In addition, network construction exhibited that circ_0008285 had 45 miRNA binding sites, which correlated with 444 mRNA. Conclusions circ_0008285 plays an important role and provides a clue for the usage of therapeutic targets in the development of GDM.

Diet and Nutritional Interventions with the Special Role of Myo-Inositol in Gestational Diabetes Mellitus Management. An Evidence-Based Critical Appraisal

2019 ◽  
Vol 25 (22) ◽  
pp. 2467-2473 ◽  
Author(s):  
Enrique Reyes-Muñoz ◽  
Federica Di Guardo ◽  
Michal Ciebiera ◽  
Ilker Kahramanoglu ◽  
Thozhukat Sathyapalan ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Metabolic Diseases ◽  
Nutritional Intervention ◽  
Attractive Alternative ◽  
Special Role ◽  
Dose Frequency ◽  
Nutritional Interventions

Background: Gestational Diabetes Mellitus (GDM), defined as glucose intolerance with onset or first recognition during pregnancy, represents one of the most common maternal-fetal complications during pregnancy and it is associated with poor perinatal outcomes. To date, GDM is a rising condition over the last decades coinciding with the ongoing epidemic of obesity and Type 2 Diabetes Mellitus (T2DM). Objective: The aim of this review is to discuss the role of diet and nutritional interventions in preventing GDM with the explanation of the special role of myo-inositol (MI) in this matter. Methods: We performed an overview of the most recent literature data on the subject with particular attention to the effectiveness of diet and nutritional interventions in the prevention of GDM with the special role of MI. Results: Nutritional intervention and physical activity before and during pregnancy are mandatory in women affected by GDM. Moreover, the availability of insulin-sensitizers such as different forms of inositol has dramatically changed the scenario, allowing the treatment of several metabolic diseases, such as those related to glucose dysbalance. Although the optimal dose, frequency, and form of MI administration need to be further investigated, diet supplementation with MI appears to be an attractive alternative for the GDM prevention as well as for the reduction of GDM-related complications. Conclusion: More studies should be conducted to prove the most effective nutritional intervention in GDM. Regarding the potential effectiveness of MI, further evidence in multicenter, randomized controlled trials is needed to draw firm conclusions.

MiR-455-5p serves as a biomarker of atherosclerosis and inhibits vascular smooth muscle cell proliferation and migration

2021 ◽  
Author(s):  
Xiang Zhang ◽  
Yan Liu ◽  
Jing Zhao ◽  
Tingguo Yan
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Diagnostic Value ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Clinical Value ◽  
Gene Assay ◽  
And Migration ◽  
Clinical Experiments ◽  
Proliferation And Migration

Background: This study discussed the clinical value and expression level of miR-455-5p in atherosclerosis (AS) patients. Meanwhile, its regulatory effect on the proliferation and migration of vascular smooth muscle cells (VSMCs) was further analyzed. Materials & methods: Clinical experiments were detected by quantitative real-time PCR and receiver operating characteristic. Cell experiments were detected by CCK-8, transwell and luciferase reporter gene assay. Results: miR-455-5p was low expressed in AS patients and had diagnostic value to distinguish AS patients from healthy controls. MiR-455-5p inhibited the proliferation and migration of VSMCs. SOCS3 was the target gene of miR-455-5p. Conclusion: MiR-455-5p may be used as a potential diagnostic biomarker for AS. MiR-455-5p may inhibit the proliferation and migration of VSMCs through targeting SOCS3.

scholarly journals The Role of IL-37 and IL-38 in Obstetrics Abnormalities

2021 ◽  
Vol 8 ◽  
Author(s):  
Mei Wang
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Inflammatory Mediator ◽  
Inflammatory Responses ◽  
Medical Practitioners ◽  
Minimal Difference ◽  
Anti Inflammatory ◽  
Umbilical Cords

There are two fairly common complications during pregnancy, i.e., gestational diabetes mellitus (GDM) and pre-eclampsia, which are independent, but are also closely linked in prevalence in pregnant women, with potential serious adverse consequences. IL-37 and IL-38, which belong to the IL-1 superfamily, participate in anti-inflammatory responses. Dysregulation of IL-37 and IL-38 has been observed in many auto-immune diseases. IL-37 is substantially reduced in the umbilical cords and placentas of GDM subjects, but IL-37 is significantly induced in the placentas of pre-eclampsia patients, suggesting there are differential regulatory roles of IL-37 in obstetrics, despite IL-37 being an anti-inflammatory mediator. Furthermore, IL-38 is substantially increased in the umbilical cords and placentas of GDM subjects, but minimal difference is observed in the placentas from pre-eclampsia patients. These data imply that IL-38 is also regulated independently within the diseased placentas. This review provides some insight for both basic scientists and medical practitioners to manage these patients effectively.

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