scholarly journals CAV1 and VCL are Downregulated in Atherosclerotic Aortic Endothelial

2021 ◽  
Author(s):  
Wei Zhang ◽  
Jianping WU ◽  
Jinyun Dong ◽  
Wenwen LI ◽  
Xinjie Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Gene Expression Omnibus ◽  
Atherosclerotic Vascular Disease ◽  
Hub Genes ◽  
Data Set ◽  
Aortic Endothelial Cells ◽  
Protein Protein Interaction ◽  
Novel Biomarkers ◽  
Arterial Endothelial Cells ◽  
Aortic Endothelial

Abstract Background: Atherosclerosis (AS) is a common atherosclerotic vascular disease, and is one of the important factors leading to cardiovascular and cerebrovascular diseases.So far, the specific etiology and pathogenesis of AS have not been clarified, and further research is needed.Methods: Bioinformatics methods were used to analyze the data set of GSE57691 and GSE137578 in normal and atherosclerotic arterial endothelial cells from Gene Expression Omnibus (GEO).Results: There are a total of 300 differentially expressed genes (DEGs) in the GSE57691 and GSE137578 datasets, which are mainly enriched in the focal adhesion signaling pathway (adj P<0.05).We identified 10 hub genes (ACTG2, CAV1, CALD1, CDC42, CCT2, CCT3, VCL, PPARG, POLR2F and TPM3) in the protein-protein interaction (PPI) network, of which 3 (CAV1, CDC42 and VCL) Significantly enriched in the adhesion signaling pathway.In addition, a search in the BIOGPS database found that CAV1 and VCL are highly expressed in coronary arteries.Conclusions: In conclusion, bioinformatics technology has proved to be useful for screening and identifying novel biomarkers of diseases.300 DEGs and 10 hub genes were significantly enriched in atherosclerotic aortic endothelial cells, especially CAV1 and VCL genes.

scholarly journals CAV1 and VCL are Downregulated in Atherosclerotic Aortic Endothelial

2021 ◽  
Author(s):  
wei zhang ◽  
Jianping Wu ◽  
Jinyun Dong ◽  
Wenwen Li ◽  
Xinjie Wang
Keyword(s):  
Endothelial Cells ◽  
Gene Expression Omnibus ◽  
Atherosclerotic Vascular Disease ◽  
Hub Genes ◽  
Data Set ◽  
Aortic Endothelial Cells ◽  
Protein Protein Interaction ◽  
Novel Biomarkers ◽  
Arterial Endothelial Cells ◽  
Aortic Endothelial

Abstract Background: Atherosclerosis (AS) is a common atherosclerotic vascular disease, and is one of the important factors leading to cardiovascular and cerebrovascular diseases.So far, the specific etiology and pathogenesis of AS have not been clarified, and further research is needed.Methods: Bioinformatics methods were used to analyze the data set of GSE57691 and GSE137578 in normal and atherosclerotic arterial endothelial cells from Gene Expression Omnibus (GEO).Results: There are a total of 300 differentially expressed genes (DEGs) in the GSE57691 and GSE137578 datasets, which are mainly enriched in the focal adhesion signaling pathway (adj P<0.05).We identified 10 hub genes (ACTG2, CAV1, CALD1, CDC42, CCT2, CCT3, VCL, PPARG, POLR2F and TPM3) in the protein-protein interaction (PPI) network, of which 3 ( CAV1, CDC42 and VCL) Significantly enriched in the adhesion signaling pathway.In addition, a search in the BIOGPS database found that CAV1 and VCL are highly expressed in coronary arteries.Conclusions: In conclusion, bioinformatics technology has proved to be useful for screening and identifying novel biomarkers of diseases.300 DEGs and 10 hub genes were significantly enriched in atherosclerotic aortic endothelial cells, especially CAV1 and VCL genes.

Immune-Related Hub Genes and the Competitive Endogenous RNA Network in Alzheimer’s Disease

2020 ◽  
Vol 77 (3) ◽  
pp. 1255-1265
Author(s):  
Hui Xu ◽  
Jianping Jia
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Expression Omnibus ◽  
Differentially Expressed ◽  
Hub Genes ◽  
Data Set ◽  
Protein Protein Interaction ◽  
Ppi Networks ◽  
Immune Phenomena ◽  
Competitive Endogenous Rna

Background: The pathogenesis of Alzheimer’s disease (AD) involves various immune-related phenomena; however, the mechanisms underlying these immune phenomena and the potential hub genes involved therein are unclear. An understanding of AD-related immune hub genes and regulatory mechanisms would help develop new immunotherapeutic targets. Objective: The aim of this study was to explore the hub genes and the mechanisms underlying the regulation of competitive endogenous RNA (ceRNA) in immune-related phenomena in AD pathogenesis. Methods: We used the GSE48350 data set from the Gene Expression Omnibus database and identified AD immune-related differentially expressed RNAs (DERNAs). We constructed protein–protein interaction (PPI) networks for differentially expressed mRNAs and determined the degree for screening hub genes. By determining Pearson’s correlation coefficient and using StarBase, DIANA-LncBase, and Human MicroRNA Disease Database (HMDD), the AD immune-related ceRNA network was generated. Furthermore, we assessed the upregulated and downregulated ceRNA subnetworks to identify key lncRNAs. Results: In total, 552 AD immune-related DERNAs were obtained. Twenty hub genes, including PIK3R1, B2M, HLA-DPB1, HLA-DQB1, PIK3CA, APP, CDC42, PPBP, C3AR1, HRAS, PTAFR, RAB37, FYN, PSMD1, ACTR10, HLA-E, ARRB2, GGH, ALDOA, and VAMP2 were identified on PPI network analysis. Furthermore, upon microRNAs (miRNAs) inhibition, we identified LINC00836 and DCTN1-AS1 as key lncRNAs regulating the aforementioned hub genes. Conclusion: AD-related immune hub genes include B2M, FYN, PIK3R1, and PIK3CA, and lncRNAs LINC00836 and DCTN1-AS1 potentially contribute to AD immune-related phenomena by regulating AD-related hub genes.

scholarly journals Identification of Hub Genes Associated With Sensitivity of 5-Fluorouracil Based Chemotherapy for Colorectal Cancer by Integrated Bioinformatics Analysis

2021 ◽  
Vol 11 ◽  
Author(s):  
Ya Wang ◽  
Qunhui Wei ◽  
Yuqiao Chen ◽  
Shichao Long ◽  
Yuanbing Yao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Colorectal Adenocarcinoma ◽  
Malignant Tumors ◽  
Gene Expression Omnibus ◽  
Chemotherapy Response ◽  
Intrinsic Resistance ◽  
Hub Genes ◽  
Protein Protein Interaction ◽  
Novel Biomarkers

Colorectal cancer (CRC) is one of the most common malignant tumors. 5-fluorouracil (5-FU) has been used for the standard first-line treatment for CRC patients for several decades. Although 5-FU based chemotherapy has increased overall survival (OS) of CRC patients, the resistance of CRC to 5-FU based chemotherapy is the principal cause for treatment failure. Thus, identifying novel biomarkers to predict response to 5-FU based chemotherapy is urgently needed. In the present study, the gene expression profile of GSE3964 from the Gene Expression Omnibus database was used to explore the potential genes related to intrinsic resistance to 5-FU. A gene module containing 81 genes was found to have the highest correlation with chemotherapy response using Weighted Gene Co-expression Network Analysis (WGCNA). Then a protein-protein interaction (PPI) network was constructed and ten hub genes (TGFBI, NID, LEPREL2, COL11A1, CYR61, PCOLCE, IGFBP7, COL4A2, CSPG2, and VTN) were identified using the CytoHubba plugin of Cytoscape. Seven of these hub genes showed significant differences in expression between chemotherapy-sensitive and chemotherapy-resistant samples. The prognostic value of these seven genes was evaluated using TCGA COAD (Colorectal Adenocarcinoma) data. The results showed that TGFBI was highly expressed in chemotherapy-sensitive patients, and patients with high TGFBI expression have better survival.

scholarly journals Identification of Key Pathways and Genes in SARS-CoV-2 Infecting Human Intestines by Bioinformatics Analysis

2021 ◽  
Author(s):  
Ji-Chun Chen ◽  
Tian-Ao Xie ◽  
Zhen-Zong Lin ◽  
Yi-Qing Li ◽  
Yu-Fei Xie ◽  
...  
Keyword(s):  
Gene Expression ◽  
Digestive Tract ◽  
Bioinformatics Analysis ◽  
Gene Expression Omnibus ◽  
Hub Genes ◽  
Data Set ◽  
Alcoholic Fatty Liver ◽  
Protein Protein Interaction ◽  
Human Digestive Tract ◽  
Gene Expression Profile Data

AbstractCOVID-19 is a serious infectious disease that has recently swept the world, and research on its causative virus, SARS-CoV-2, remains insufficient. Therefore, this study uses bioinformatics analysis techniques to explore the human digestive tract diseases that may be caused by SARS-CoV-2 infection. The gene expression profile data set, numbered GSE149312, is from the Gene Expression Omnibus (GEO) database and is divided into a 24-h group and a 60-h group. R software is used to analyze and screen out differentially expressed genes (DEGs) and then gene ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses are performed. In KEGG, the pathway of non-alcoholic fatty liver disease exists in both the 24-h group and 60-h group. STRING is used to establish a protein–protein interaction (PPI) network, and Cytoscape is then used to visualize the PPI and define the top 12 genes of the node as the hub genes. Through verification, nine statistically significant hub genes are identified: AKT1, TIMP1, NOTCH, CCNA2, RRM2, TTK, BUB1B, KIF20A, and PLK1. In conclusion, the results of this study can provide a certain direction and basis for follow-up studies of SARS-CoV-2 infection of the human digestive tract and provide new insights for the prevention and treatment of diseases caused by SARS-CoV-2.

Effect of Volatile Anesthetics on Hydrogen Peroxide-induced Injury in Aortic and Pulmonary Arterial Endothelial Cells

1996 ◽  
Vol 84 (1) ◽  
pp. 103-116 ◽  
Author(s):  
Michael E. Johnson ◽  
Christopher J. Sill ◽  
Cindy B. Uhl ◽  
Teresa J. Halsey ◽  
Gregory J. Gores
Keyword(s):  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Cell Death ◽  
Volatile Anesthetics ◽  
Cytosolic Calcium ◽  
Oxidant Injury ◽  
Aortic Endothelial Cells ◽  
Pulmonary Arterial ◽  
Arterial Endothelial Cells ◽  
Aortic Endothelial

Background Oxidant damage to endothelial cells occurs during inflammation and reperfusion after ischemia, mediated in part by endogenously produced hydrogen peroxide (H2O2). Previous studies have established a role for increased cytosolic calcium in the mechanism of endothelial oxidant injury, and have suggested that volatile anesthetics may exacerbate oxidant injury in pulmonary endothelium. However, the effect of volatile anesthetics on oxidant injury to systemic arterial endothelial cells, and their effect on oxidant-related changes in cytosolic calcium homeostasis, have not been reported previously. Methods Primary cultures of human aortic and pulmonary arterial endothelial cells were studied. The rate of cell death after H2O2 exposure was determined in cell suspension by propidium iodide fluorimetry and lactate dehydrogenase release. The final extent of cell death 24 h after H2O2 exposure was determined in monolayer cultures by methyl thiazolyl tetrazolium reduction. Cytosolic calcium and cell death were determined in single cells using fura-2 and propidium iodide imaging with digitized, multiparameter, fluorescent video microscopy. Results In aortic endothelial cells, clinical concentrations of halothane (1.0%) and isoflurane (1.5%) decreased both the rate of cell death and the final extent of cell death after H2O2 exposure, with halothane being more protective. Supraclinical concentrations of halothane (2.7%) and isoflurane (4.0%) were less protective. In pulmonary arterial endothelial cells, halothane and isoflurane had essentially no effect on H2O2-mediated cell death. The protective effect of anesthetic in aortic endothelial cells was not due to an enhanced removal of H2O2 by endogenous enzymes. Hydrogen peroxide exposure caused a large increase in cytosolic calcium well before cell death, and this was moderated by anesthetic treatment. Conclusions The effect of volatile anesthetics on oxidant injury to endothelial cells may differ between cells derived from systemic and pulmonary vascular beds. Halothane, and to a lesser extent, isoflurane, protects against oxidant injury in aortic endothelial cells. The mechanism of protection may involve modulation of the interaction of H2O2 with vital cellular constituents, and/or amelioration of the toxic increase in cytosolic calcium that follows such interaction.

Effects of Dipyrone on Prostaglandin Production by Human Platelets and Cultured Bovine Aortic Endothelial Cells

1983 ◽  
Vol 49 (02) ◽  
pp. 132-137 ◽  
Author(s):  
A Eldor ◽  
G Polliack ◽  
I Vlodavsky ◽  
M Levy
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Competitive Inhibition ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

SummaryDipyrone and its metabolites 4-methylaminoantipyrine, 4-aminoantipyrine, 4-acetylaminoantipyrine and 4-formylaminoan- tipyrine inhibited the formation of thromboxane A2 (TXA2) during in vitro platelet aggregation induced by ADP, epinephrine, collagen, ionophore A23187 and arachidonic acid. Inhibition occurred after a short incubation (30–40 sec) and depended on the concentration of the drug or its metabolites and the aggregating agents. The minimal inhibitory concentration of dipyrone needed to completely block aggregation varied between individual donors, and related directly to the inherent capacity of their platelets to synthesize TXA2.Incubation of dipyrone with cultured bovine aortic endothelial cells resulted in a time and dose dependent inhibition of the release of prostacyclin (PGI2) into the culture medium. However, inhibition was abolished when the drug was removed from the culture, or when the cells were stimulated to produce PGI2 with either arachidonic acid or ionophore A23187.These results indicate that dipyrone exerts its inhibitory effect on prostaglandins synthesis by platelets or endothelial cells through a competitive inhibition of the cyclooxygenase system.

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