scholarly journals The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10803
Author(s):  
Changlin Qian ◽  
Weiqing Qiu ◽  
Jie Zhang ◽  
Zhiyong Shen ◽  
Hua Liu ◽  
...  
Keyword(s):  
Normal Control ◽  
Regulatory Network ◽  
Cholesterol Gallstone ◽  
Normal Control Group ◽  
Differentially Expressed ◽  
Pcr Analysis ◽  
Control Group ◽  
Ppi Network ◽  
Model Group ◽  
Qrt Pcr

Background Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. Methods Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. Results The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. Conclusion These RNAs might be related to the pathogenesis of CG.

scholarly journals The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone

2020 ◽  
Author(s):  
Changlin Qian ◽  
Hua Liu ◽  
Weijing Qiu ◽  
Jie Zhang ◽  
Zhiyong Shen ◽  
...  
Keyword(s):  
Normal Control ◽  
Regulatory Network ◽  
Cholesterol Gallstone ◽  
Gallstone Disease ◽  
Lipid Hydroperoxide ◽  
Normal Control Group ◽  
Differentially Expressed ◽  
Control Group ◽  
Ppi Network ◽  
Model Group

Abstract Background: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. Methods: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using clusterProfiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Results: The mouse model of CG was successfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were selected. For the down-regulated SCP2 , lipid hydroperoxide transport was enriched. Moreover, KDM4A was selected as a hub node in the PPI network, and MEG3 was taken as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3p—MEG3 regulatory pairs and MEG3—PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. Conclusion: These RNAs might be related to the pathogenesis of CG.

scholarly journals Study on potential differentially expressed genes in stroke by bioinformatics analysis

2021 ◽  
Author(s):  
Xitong Yang ◽  
Pengyu Wang ◽  
Shanquan Yan ◽  
Guangming Wang
Keyword(s):  
Gene Expression ◽  
Differentially Expressed Genes ◽  
Normal Control ◽  
Enrichment Analysis ◽  
Normal Control Group ◽  
Control Group ◽  
Ppi Network ◽  
Hub Genes ◽  
Pathway Enrichment ◽  
Key Genes

AbstractStroke is a sudden cerebrovascular circulatory disorder with high morbidity, disability, mortality, and recurrence rate, but its pathogenesis and key genes are still unclear. In this study, bioinformatics was used to deeply analyze the pathogenesis of stroke and related key genes, so as to study the potential pathogenesis of stroke and provide guidance for clinical treatment. Gene Expression profiles of GSE58294 and GSE16561 were obtained from Gene Expression Omnibus (GEO), the differentially expressed genes (DEGs) were identified between IS and normal control group. The different expression genes (DEGs) between IS and normal control group were screened with the GEO2R online tool. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the DEGs were performed. Using the Database for Annotation, Visualization and Integrated Discovery (DAVID) and gene set enrichment analysis (GSEA), the function and pathway enrichment analysis of DEGS were performed. Then, a protein–protein interaction (PPI) network was constructed via the Search Tool for the Retrieval of Interacting Genes (STRING) database. Cytoscape with CytoHubba were used to identify the hub genes. Finally, NetworkAnalyst was used to construct the targeted microRNAs (miRNAs) of the hub genes. A total of 85 DEGs were screened out in this study, including 65 upward genes and 20 downward genes. In addition, 3 KEGG pathways, cytokine − cytokine receptor interaction, hematopoietic cell lineage, B cell receptor signaling pathway, were significantly enriched using a database for labeling, visualization, and synthetic discovery. In combination with the results of the PPI network and CytoHubba, 10 hub genes including CEACAM8, CD19, MMP9, ARG1, CKAP4, CCR7, MGAM, CD79A, CD79B, and CLEC4D were selected. Combined with DEG-miRNAs visualization, 5 miRNAs, including hsa-mir-146a-5p, hsa-mir-7-5p, hsa-mir-335-5p, and hsa-mir-27a- 3p, were predicted as possibly the key miRNAs. Our findings will contribute to identification of potential biomarkers and novel strategies for the treatment of ischemic stroke, and provide a new strategy for clinical therapy.

scholarly journals Improvement of Electroacupuncture on APP/PS1 Transgenic Mice in Spatial Learning and Memory Probably due to Expression of Aβand LRP1 in Hippocampus

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Xin Wang ◽  
Yanhuan Miao ◽  
Jiawula Abulizi ◽  
Fu Li ◽  
Yuping Mo ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Normal Control ◽  
Water Maze ◽  
Normal Control Group ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Model Group ◽  
Amyloid A

Objectives. To explore the alterations ofβ-amyloid (Aβ) and low density lipoprotein receptor-related protein-1 (LRP1) in APP/PS1 mice after electroacupuncture (EA) treatment and further to explore the mechanism.Methods. Forty 6-month-old APP/PS1 mice were randomly divided into a model group and an EA group, with twenty wild-type mice used as a normal control group. Mice in the EA group were treated with EA at GV 20 (băi huì) and bilateral KI 1 (yŏng quán) acupoints for 6 weeks. The Morris water maze was applied to assess the spatial memory in behavior. Immunohistochemistry (IHC), ELISA, Western blotting, and so forth were used to observe the expression of LRP1 and Aβ.Results. The Morris water maze test showed that, compared with the normal control group, the model group’s learning and memory capabilities were significantly decreased (P<0.05;P<0.01). The EA group was reversed (P<0.05;P<0.01). The hippocampal expression of Aβin the EA group was significantly decreased compared to the model group (P<0.01). The expression of LRP1 in the model group was significantly lower than that in the normal control group (P<0.01); the expression in the EA group was significantly higher than that in the model group (P<0.01).Conclusions. EA therapy can improve the learning and memory capabilities of APP/PS1 mice. The underlying mechanism may lie in the upregulation of an Aβtransport receptor and LRP1.

scholarly journals MicroRNA-34a alleviates steroid-induced avascular necrosis of femoral head by targeting Tgif2 through OPG/RANK/RANKL signaling pathway

2017 ◽  
Vol 242 (12) ◽  
pp. 1234-1243 ◽  
Author(s):  
Wu-Xun Peng ◽  
Chuan Ye ◽  
Wen-Tao Dong ◽  
Lei-Luo Yang ◽  
Chun-Qing Wang ◽  
...  
Keyword(s):  
Femoral Head ◽  
Signaling Pathway ◽  
Normal Control ◽  
Normal Control Group ◽  
Control Group ◽  
Micro Ct ◽  
Model Group ◽  
Model Control ◽  
Model Control Group ◽  
Necrosis Of Femoral Head

The study aims to investigate the effect of microRNA-34a (miR-34a) targeting Tgif2 on steroid-induced avascular necrosis of femoral head (SANFH) by regulating OPG/RANK/RANKL signaling pathway. SD rats were divided into normal control and model (RNAKL rat models) groups. The model group was further assigned into model control, negative control, miR-34a mimics and miR-34a inhibitors groups. QRT-PCR was applied to detect miR-34a, Tgif2, OPG, RANK and RNAKL mRNA expressions. Femoral head tissues were collected for Micro-CT scanning and HE staining. QRT-PCR and Western blotting were used to detect expressions of miR-34a, Tgif2, OPG, RANK, RANKL and Runx2, OPN and OC in bone tissues. Dual-luciferase reporter gene assay was used to testify the target relationship between miR-34a and Tgif2. Compared with the normal control group, the model group showed increased Tgif2, RANK and RANKL mRNA expressions, but decreased miR-34a and OPG mRNA expressions. Tgif2 mRNA expression was negatively correlated with miR-34a and OPG mRNA expressions. Micro-CT showed cystic degeneration of femoral head, with decreased bone volume/total volume (BV/TV), bone surface area/bone volume and trabecular number in the model control group compared with the normal control group. Compared with the model control group, the miR-34a mimics group showed increased BV/TV and trabecular thickness and Runx2, OPN and OC expressions, while the parameters decreased in the miR-34a inhibitors group. Compared with the normal control group, the other groups showed increased Tgif2, RANK and RANKL expressions but decreased miR-34a and OPG expressions. Compared with the model control group, Tgif2, RANK and RANKL expressions decreased and miR-34a and OPG expressions increased in the miR-34a mimics group, while the miR-34a inhibitors group had a reverse trend in contrast to the miR-34a mimics group. Tgif2 is a target gene of miR-34a. In conclusion, miR-34a can alleviate SANFH through targeting Tgif2 and further regulating OPG/RANK/RANKL signaling pathway. Impact statement miR-34a can alleviate SANFH through targeting Tgif2 and further regulating OPG/RANK/RANKL signaling pathway, which can be used as a new theoretical basis for SANFH treatment.

scholarly journals Study on the Effect of Macrophages on Vascular Endothelium in Mice With Different TCM Syndromes of Dyslipidemia and its Biological Basis Based on RNA-Seq Technology

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Chen ◽  
Chao Ye ◽  
Zheng Yang ◽  
Tieshan Wang ◽  
Bing Xu ◽  
...  
Keyword(s):  
Quality Assessment ◽  
Differentially Expressed Genes ◽  
Normal Control ◽  
Normal Control Group ◽  
Differentially Expressed ◽  
Control Group ◽  
Biological Processes ◽  
Rna Seq ◽  
Pathogenic Factors ◽  
Protective Processes

Background: “Treating the same disease with different methods” is a Traditional Chinese medicine (TCM) therapeutic concept suggesting that, while patients may be diagnosed with the same disease, they may also have different syndromes that require distinct drug administrations.Objective: This study aimed to identify the differentially expressed genes and related biological processes in dyslipidemia in relation to phlegm–dampness retention (PDR) syndrome and spleen and kidney Yang deficiency (SKYD) syndrome using transcriptomic analysis.Methods: Ten ApoE−/− mice were used for the establishment of dyslipidemic disease–syndrome models via multifactor-hybrid modeling, with five in the PDR group and five in the SKYD group. Additionally, five C57BL/6J mice were employed as a normal control group. Test model-quality aortic endothelial macrophages in mice were screened using flow cytometry. Transcriptomic analysis was performed for macrophages using RNA-Seq.Results: A quality assessment of the disease–syndrome model showed that levels of lipids significantly increased in the PDR and SKYD groups, compared to the normal control group, p &lt; 0.05. Applying, in addition, hematoxylin and eosin staining of aorta, the disease model was also successfully established. A quality assessment of the syndrome models showed that mice in the PDR group presented with typical manifestations of PDR syndrome, and mice in the SKYD group had related manifestations of SKYD syndrome, indicating that the syndrome models were successfully constructed as well. After comparing the differentially expressed gene expressions in macrophages of the dyslipidemic mice with different syndromes, 4,142 genes were identified with statistical significance, p &lt; 0.05. Gene ontology analysis for the differentially expressed genes showed that the biological process of difference between the PDR group and the SKYD group included both adverse and protective processes.Conclusion: The differentially expressed genes between PDR syndrome and SKYD syndrome indicate different biological mechanisms between the onsets of the two syndromes. They have distinctive biological processes, including adverse and protective processes that correspond to the invasion of pathogenic factors into the body and the fight of healthy Qi against pathogenic factors, respectively, according to TCM theory. Our results provide biological evidence for the TCM principle of “treating the same disease with different treatments.”

scholarly journals Corn silk polysaccharide ameliorates high fat diet induced hepatic steatosis in mice

2021 ◽  
Vol 271 ◽  
pp. 03027
Author(s):  
Wang Tailin ◽  
Wang Zhiwen ◽  
Liu Yi ◽  
Huang Li
Keyword(s):  
Food Intake ◽  
Normal Control ◽  
High Fat Diet ◽  
Statistical Significance ◽  
Normal Control Group ◽  
Control Group ◽  
Model Group ◽  
High Fat ◽  
Corn Silk ◽  
Intake Water

To study the therapeutic effect of corn silk polysaccharide (CSP) on NAFLD mice induced by high fat diet. C57BL/6J mice were divided into normal control group (NC), high fat diet (HFD) group, HFD+200 mg/kg CSP group, and HFD+600 mg/kg CSP group. NAFLD mouse model was established by HFD feeding. Blood and liver tissues of each group were collected and biochemical and pathological tests were performed. The energy intake of NAFLD model group was higher than that of normal control group, and the food intake, water intake, and excretion of NAFLD model group were lower than that of normal control group. There was no statistical significance in the food intake, energy intake, water intake, and excretion of CSP group compared with that of NAFLD model group, nor was there any statistical significance between CSP and two doses of CSP. Biochemical tests showed that CSP decreased the levels of alanine aminotransferase, aspartate aminotransferase, triglyceride and total cholesterol in serum of HFDfed mice, and inhibited the expressions of IL-6 and TNF-α in liver tissue. Pathological results showed that CSP improved HFD-induced hepatic steatosis.

scholarly journals Effect of Angiotensin 1-7 on Myocardial Calcium Pump in Salt-Sensitive Hypertensive Rats

2021 ◽  
Vol 2 (3) ◽  
Author(s):  
Jun Cao ◽  
Qianfeng Jiang ◽  
Mingliang Fang
Keyword(s):  
Normal Control ◽  
Early Stage ◽  
Sensory Nerve ◽  
Normal Control Group ◽  
Calcium Pump ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Model Group ◽  
Plasma Membrane Atpase ◽  
Hypertensive Rats

Objective — To investigate the effects of angiotensin 1-7 (Ang1-7) on plasma membrane ATPase isoform 1 (PMCA1) in salt-sensitive hypertensive rats. Methods — Thirty newborn male Wistar rats were selected to establish the salt-sensitive hypertensive rat model with sensory nerve injury, which were then randomly divided into 5 groups (n=5), including model group, Telmisartan group, Ramipril group, Ang1-7 group, and A-779 group. Another normal control group was established (n=5). After 4 weeks of intervention, the tail blood pressure of rats in each group was measured, and then the apical tissue of left ventricle was cut. The contents of AngⅡ and Ang1-7 in cardiomyocytes were detected by enzyme-linked immunosorbent assay. The expression of PMCA1 mRNA and protein in heart of salt-sensitive hypertensive rats were detected by RT-PCR and immunohistochemistry. Results — (1) Compared with the normal control group, the concentration of AngⅡ in the myocardium of salt-sensitive hypertensive rats increased (P < 0.05), which decreased after the intervention of Telmisartan and Ramipril (P < 0.05), and no change occurred after the intervention of Ang1-7 in concentration (P＞0.05). (2) Compared with the normal control group, the concentration of myocardial Ang1-7 in salt-sensitive hypertensive rats decreased (P < 0.05), and increased after the intervention of telmisartan and ramipril (P < 0.05), and increased after the intervention of A-779 (P < 0.05). (3) The expression of PMCA1 mRNA and protein in salt-sensitive hypertensive rats was increased compared with the normal control group (P < 0.05), and the expression of Ang-(1-7), telmisartan and ramipril was decreased compared with the model group (P < 0.05). The expression of p38MAPK mRNA and p-p38MAPK protein in the myocardium of salt-sensitive hypertensive rats was increased compared with that in the normal control group (P < 0.05), and the expression of Ang-(1-7), Telmisartan and Ramipril was decreased compared with that in the model group (P < 0.05). Conclusion — Ang-(1-7) may be involved in the regulation of cardiac calcium pump, inhibiting its overcompensation and delaying the occurrence of calcium pump inhibition in the early stage of salt-sensitive hypertension. Ang-(1-7) can inhibit the activity of p38MAPK and protect the heart, and its regulation on PMCA1 may be mediated by the expression of p38MAPK pathway.

scholarly journals ITRAQ-based quantitative proteomic analysis of Fusarium moniliforme (Fusarium verticillioides) in response to Phloridzin inducers

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Rong Zhang ◽  
Weitao Jiang ◽  
Xin Liu ◽  
Yanan Duan ◽  
Li Xiang ◽  
...  
Keyword(s):  
Fusarium Moniliforme ◽  
Abiotic Factors ◽  
Fusarium Verticillioides ◽  
Protein Profile ◽  
Sugar Metabolism ◽  
Differentially Expressed ◽  
Pcr Analysis ◽  
Differentially Expressed Proteins ◽  
Apple Replant Disease ◽  
Qrt Pcr

Abstract Background Apple replant disease (ARD) has been reported from all major fruit-growing regions of the world, and is often caused by biotic factors (pathogen fungi) and abiotic factors (phenolic compounds). In order to clarify the proteomic differences of Fusarium moniliforme under the action of phloridzin, and to explore the potential mechanism of F. moniliforme as the pathogen of ARD, the role of Fusarium spp. in ARD was further clarified. Methods In this paper, the quantitative proteomics method iTRAQ analysis technology was used to analyze the proteomic differences of F. moniliforme before and after phloridzin treatment. The differentially expressed protein was validated by qRT-PCR analysis. Results A total of 4535 proteins were detected, and 293 proteins were found with more than 1.2 times (P< 0.05) differences. In-depth data analysis revealed that 59 proteins were found with more than 1.5 times (P< 0.05) differences, and most proteins were consistent with the result of qRT-PCR. Differentially expressed proteins were influenced a variety of cellular processes, particularly metabolic processes. Among these metabolic pathways, a total of 8 significantly enriched KEGG pathways were identified with at least 2 affiliated proteins with different abundance in conidia and mycelium. Functional pathway analysis indicated that up-regulated proteins were mainly distributed in amino sugar, nucleotide sugar metabolism, glycolysis/ gluconeogenesis and phagosome pathways. Conclusions This study is the first to perform quantitative proteomic investigation by iTRAQ labeling and LC-MS/MS to identify differentially expressed proteins in F. moniliforme under phloridzin conditions. The results confirmed that F. moniliforme presented a unique protein profile that indicated the adaptive mechanisms of this species to phloridzin environments. The results deepened our understanding of the proteome in F. moniliforme in response to phloridzin inducers and provide a basis for further exploration for improving the efficiency of the fungi as biocontrol agents to control ARD.

Effect of GDM on the Expression of MT1-MMP and u-PA in Glioma Cells

2014 ◽  
Vol 1033-1034 ◽  
pp. 220-223
Author(s):  
Xue Mei Han ◽  
Li Bo Wang ◽  
Ni Ni Li ◽  
Song Yan Liu
Keyword(s):  
Normal Control ◽  
Glioma Cell ◽  
Fetal Bovine Serum ◽  
Glioma Cells ◽  
Normal Control Group ◽  
Control Group ◽  
Rt Pcr ◽  
Glioma Cell Lines ◽  
Fetal Bovine ◽  
Identify Gene Expression

To examine the effect of GDM on the expression of MT1-MMP and u-PA genes in glioma cells. Glioma cell lines U251 and U87 were cultured in DMEM medium supplemented with 10% fetal bovine serum. RT-PCR was used to identify gene expression level. The level of u-PA mRNA was up-regulated significantly in the HGF group compared with the normal control group (P<0.05). The expression of MT1-MMP and u-PA was significantly lower in the GDM group than in the normal control and HGF groups (P<0.05). The expression of u-PA in the HGF+GDM group was down-regulated significantly compared with the normal control and HGF groups (P<0.05).GDM can inhibit expression of both MT1-MMP and u-PA in glioma cells.

Identification of Hub Genes Associated with Development of Lung Adenocarcinoma by Integrated Bioinformatics Analysis

2021 ◽  
Author(s):  
Jinglei Li ◽  
Wei Hou
Keyword(s):  
Gene Expression ◽  
Survival Analysis ◽  
Network Analysis ◽  
Lung Adenocarcinoma ◽  
Normal Control ◽  
Gene Expression Analysis ◽  
Normal Control Group ◽  
Control Group ◽  
Differential Gene Expression Analysis ◽  
Differential Gene

Abstract Purpose: Lung adenocarcinoma (LUAD) has high heterogeneity and poor prognosis, posing a major challenge to human health worldwide. Therefore, it is necessary to improve our understanding of the molecular mechanism of LUAD in order to be able to better predict its prognosis and develop new therapeutic strategies for target genes.Methods: The Cancer Genome Atlas and Gene Expression Omnibus, were selected to comprehensively analyze and explore the differences between LUAD tumors and adjacent normal tissues. Critical gene information was obtained through weighted gene co-expression network analysis (WGCNA), differential gene expression analysis, and survival analysis.Results: Using WGCNA and differential gene expression analysis, 29 differentially expressed genes were screened. The functional annotation analysis showed these genes to be mainly concentrated in heart trabecula formation, regulation of inflammatory response, collagen-containing extracellular matrix, and metalloendopeptidase inhibitor activity. Also, in the protein–protein interaction network analysis, 10 central genes were identified using Cytoscape's CytoHubba plug-in. The expression of CDH5, TEK, TIMP3, EDNRB, EPAS1, MYL9, SPARCL1, KLF4, and TGFBR3 in LUAD tissue was found to be lower than that in the normal control group, while the expression of MMP1 in LUAD tissue was higher than that in the normal control group. According to survival analysis, the low expression of MYL9 and SPARCL1 was correlated with poor overall survival in patients with LUAD. Finally, through the verification of the Oncomine database, it was found that the expression levels of MYL9 and SPARCL1 were consistent with the mRNA levels in LUAD samples, and both were downregulated.Conclusion: Two survival-related genes, MYL9 and SPARCL1, were determined to be highly correlated with the development of LUAD. Both may play an essential role in the development LUAD and may be potential biomarkers for its diagnosis and treatment in the future.

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