Comparison of gene expression between Human umbilical vein endothelial cells and Human liver sinusoidal endothelial cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE78020 | GEO | 2016/10/24
SECONDARY ACCESSION(S): PRJNA312370
REPOSITORIES: GEO
Similar Datasets
Project description:To identify leukocyte adhesion receptors which differentially regulate recruitment in human liver sinusoidal endothelial cells compared to a protoptypic venular endothelium Gene expression was measured in four groups Group 1: cultured human liver sinusoidal endothelial cells (HSEC) Group 2: cultured human umbilical vein endothelial cells (HUVEC) Group3: Interferon gamma and tumour necrosisfactor alpha treated HSEC and Group 4: Interferon gamma and tumour necrosisfactor alpha treated HUVEC. Two replicates were used for each group.
2016-10-24 | E-GEOD-78020 | biostudies-arrayexpress
Project description:Obesity may promote myeloid cell accumulation in liver. Intravital liver tissue imaging revealed that the number of myeloid cells attached to sinusoidal wall significantly increased in ob/ob mice. To assess the pathophysiological roll of liver sinusoidal endothelial cells (LSEC) in obese livers, we performed microarray analysis in LSEC isolated from an 8-week-old wild-type and ob/ob mouse. Pathway analysis in microarray data shows genes related to cell adhesion, chemokine signaling and leukocyte transendothelial migration are upregulated in LSEC from ob/ob.
2017-02-15 | GSE84019 | GEO
Project description:Inflammatory activation of endothelial cells enables leukocyte recruitment to tissues. We here investigate how Notch1 signaling affects the transcriptional profile of inflammatory activated human umbilical vein cells.
2018-08-29 | GSE85986 | GEO
Project description:We report the transcriptome human primary hepatocytes and liver sinusoidal endothelial cells. Hepatocytes were obtained from commercial sources. LSECs were isolated based on the coexpression of Tie2 and CD32b, te strategy of purification controlled by RNA-Seq. Comparison of the expression of the Tie-2, CD32b, SELP, FVIII, VWF, Alb, Fg, F7genes
2015-01-01 | E-GEOD-43984 | biostudies-arrayexpress
Project description:Comparison of C57BL/6J 8-10 weeks male mouse liver sinusoidal endothelial cells (LSEC) from normal liver and from liver injured by carbon tetrachloride administration. Keywords: other
2004-10-01 | E-GEOD-1689 | biostudies-arrayexpress
Project description:Background: In diabetes chronic hyperinsulinemia is responsible for the instability of the atherosclerotic plaque and stimulates cellular proliferation through the activation of the MAP kinases, which in turn regulate cellular proliferation. However, it is not known whether insulin itself could increase the transcription of specific genes for cellular proliferation in the endothelium. Hence, the characterization of transcriptional modifications in endothelium is an important step for a better understanding of the mechanism of insulin action and the relationship between endothelial cell dysfunction and insulin resistance. Methodology and principal findings: The transcriptional response of endothelial cells in the 440 minutes following insulin stimulation was monitored using microarrays and compared to a control condition. About 1700 genes were selected as differentially expressed based on their treated minus control profile, thus allowing the detection of even small but systematic changes in gene expression. Genes were clustered in 7 groups according to their time expression profile and classified into 15 functional categories that can support the biological effects of insulin, based on Gene Ontology enrichment analysis. In terms of endothelial function, the most prominent processes affected were NADH dehydrogenase activity, N-terminal myristoylation domain binding, nitric-oxide synthase regulator activity and growth factor binding. Pathway-based enrichment analysis revealed “Electron Transport Chain” significantly enriched. Results were validated on genes belonging to “Electron Transport Chain” pathway, using quantitative RT-PCR. Conclusions: As far as we know, this is the first systematic study in the literature monitoring transcriptional response to insulin in endothelial cells, in a time series microarray experiment. Since chronic hyperinsulinemia is responsible for the instability of the atherosclerotic plaque and stimulates cellular proliferation, some of the genes identified in the present work are potential novel candidates in diabetes complications related to endothelial dysfunction.
2010-05-26 | GSE21989 | GEO
Project description:We report the transcriptome human primary hepatocytes and liver sinusoidal endothelial cells. Hepatocytes were obtained from commercial sources. LSECs were isolated based on the coexpression of Tie2 and CD32b, te strategy of purification controlled by RNA-Seq.
2015-01-01 | GSE43984 | GEO
Project description:next generation RNAseq data from human hepatic sinusoidal endothelial cells and primary mouse sinusoidal endothelial cells plated on soft vs hard gels reveals the chemokine CXCL1 being among the top up-regulated genes from granulocyte and agranulocyte migration/diapedesis pathway.
2022-03-31 | GSE198462 | GEO
Project description:Background: In diabetes chronic hyperinsulinemia is responsible for the instability of the atherosclerotic plaque and stimulates cellular proliferation through the activation of the MAP kinases, which, in turn regulate cellular proliferation. So far, it is not known, however, whether insulin itself could increase the transcription of specific genes for cellular proliferation in the endothelium. Hence, the characterization of the global pattern of transcriptional modifications in endothelium is an important step for a better understanding of the mechanism of action of insulin and of its defects in situations of insulin resistance. Methodology and principal findings: The transcriptional response of endothelial cells in the eight hours following insulin stimulation was monitored using microarrays and compared to a control condition. About 1700 genes were selected as differentially expressed based on their treated minus control profile, thus allowing the detection of even small but systematic changes in gene expression. Genes were clustered in 7 groups according to their time expression profile and classified into 15 functional categories that can support the biological effects of insulin, based on Gene Ontology enrichment analysis. In terms of endothelial function, the most prominent processes affected were NADH dehydrogenase activity, N-terminal myristoylation domain binding, nitric-oxide synthase regulator activity and growth factor binding. Pathway based enrichment analysis revealed âElectron Transport Chainâ and âMatrix Metalloproteinasesâ significantly enriched. Results were validated on genes belonging to âElectron Transport Chainâ pathway, using quantitative RT-PCR. Conclusions: As far as we know, this is the first systematic study in the literature monitoring transcriptional response to insulin in endothelial cells, in a time series microarray experiment. Since chronic hyperinsulinemia is responsible for the instability of the atherosclerotic plaque and stimulates cellular proliferation, some of the genes identified in the present work are potential novel candidates in diabetes complications related to endothelial dysfunction. Experiments were carried on human umbilical venous endothelial cells (HUVEC) to elucidate the regulatory aspects of insulin from dynamic gene expression data. HUVEC incubated with or without insulin were collected at times 0', 40', 100', 200', 340' and 440'. RNA was extracted and quantified for high-density oligonucleotide microarrays Human Genome U133 Plus 2.0 GeneChip (Affymetrix, Santa Clara, CA).
2010-06-08 | E-GEOD-21989 | biostudies-arrayexpress
Project description:OBJECTIVES:Hypoxia leads to endothelial cell inflammation, apoptosis, and damage, which plays an important role in the complications associated with ischemic cardiovascular disease. As an oxidoreductase, p66Shc plays an important role in the regulation of reactive oxygen species (ROS) production and apoptosis. Ketamine is widely used in clinics. This study was designed to assess the potential protective effect of ketamine against hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs). Moreover, we explored the potential mechanism by which ketamine protected against hypoxia-induced endothelial injury. METHODS:The protective effects of ketamine against hypoxia-induced injury was assessed using cell viability and adhesion assays, quantitative polymerase chain reaction, and western blotting. RESULTS:Our data showed that hypoxia reduced HUVEC viability, increased the adhesion between HUVECs and monocytes, and upregulated the expression of endothelial adhesion molecules at the protein and mRNA levels. Moreover, hypoxia increased ROS accumulation and upregulated p66Shc expression. Furthermore, hypoxia downregulated sirt1 expression in HUVECs. Alternatively, ketamine was shown to reverse the hypoxia-mediated reduction of cell viability and increase in the adhesion between HUVECs and monocytes, ameliorate hypoxia-induced ROS accumulation, and suppress p66Shc expression. Moreover, EX527, a sirt1 inhibitor, reversed the protective effects of ketamine against the hypoxia-mediated reduction of cell viability and increase in adhesion between HUVECs and monocytes. CONCLUSION:Ketamine reduces hypoxia-induced p66Shc expression and attenuates ROS accumulation via upregulating sirt1 in HUVECs, thus attenuating hypoxia-induced endothelial cell inflammation and apoptosis.
| S-EPMC7470431 | biostudies-literature