Endothelial in vivo vs. in vitro responses to LPS
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1044 | GEO | 2004/02/26
SECONDARY ACCESSION(S): PRJNA87121
REPOSITORIES: GEO
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Project description:Endothelial responses to LPS using endothelial cells freshly isolated from Tie2 GFP animals vs. cultured cell line. This SuperSeries is composed of the SubSeries listed below.
2010-06-09 | E-GEOD-1044 | biostudies-arrayexpress
Project description:Transcriptional responses of cardiac endothelial cells isolated from Tie-2 GFP mice 4 h and 24 h after intraperitoneal LPS injection. Operon V1 long oligo set. Hybridization using Cy3 and Cy5 labeled amplified RNA. Keywords: parallel sample
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Project description:Cardiac endothelial RNA from Tie-2 GFP mice exposed to intraperitoneal LPS vs. saline, 4 h. RNA amplified 2 rounds. Experiment and dye reversal with cy5, cy3.
2010-06-09 | E-GEOD-1038 | biostudies-arrayexpress
Project description:Cardiac endothelial RNA from Tie-2 GFP mice exposed to intraperitoneal LPS vs. saline, 4 h. RNA amplified 2 rounds. Experiment and dye reversal with cy5, cy3. Keywords: parallel sample
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Project description:Endothelial dysfunction is a hallmark of LPS-induced acute kidney injury (AKI). Endothelial cells (EC) acquired a fibroblast-like phenotype and contributed to myofibroblasts generation through Endothelial to Mesenchymal Transition (EndMT) process. Noteworthy, ARPCs enhance tubular regenerative mechanism during AKI, but little is known about their effects on EC. Here we investigated whether ARPCs could prevent sepsis-induced EndMT and the related mechanism. When activated by LPS, Human endothelial cells (EC) proliferated and decreased specific EC markers such as CD31 and VE-cadherin and up-regulated myofibroblast markers such as Collagen I and Vimentin. The co-culture with ARPCs normalized EC proliferation rate and abrogated the LPS-induced EndMT by restoring the high expression of EC markers and the low expression of myofibroblast markers. Gene set enrichment analysis showed that most of genes modulated in LPS-stimulated ARPCs belongs to cell activation and defense response pathways. In particular, among most up-regulated genes we found BPIFA2, SAA2, SAA4 and CXCL6. BPIFA2 is recently described as an early biomarker of AKI but little is known about its function in the kidney. The other genes are frequently involved in the response to bacterial infection and kidney injury. Finally, in a swine model of LPS-induced AKI, we observed an increase of CD133+ARPCs that expressed BPIFA2 respect to healthy pigs. Taken together, these results suggest an underestimate role of ARPCS in preventing endothelial dysfuncton by the production of several proteins. The identification of these molecules may offer novel strategies to protect endothelial compartment and promote kidney repair.
2019-07-01 | GSE116849 | GEO
Project description:Four daily intraperitoneal injections of the Gram-negative bacterial endotoxin lipopolysaccharide (LPS) transiently protects the cerebral cortex against traumatic brain injury. Underlying mechanisms associated with this neuroprotection include increased neuronal production of anti-apoptotic and neurotrophic molecules, microglial-mediated displacement of inhibitory presynaptic terminals innervating the soma of cortical projection neurons, and synchronized firing of cortical projection neurons. The molecular mechanisms responsible for inducing this neuroprotection and microglial activation are unknown. A fundamental question is whether LPS enters the central nervous system (CNS) or mediates it actions on the luminal surface of brain endothelial cells. In this study, we demonstrate that LPS injected into the peritoneum does not enter the CNS or alter tight junctions of brain endothelial cells. However, LPS activation of vascular endothelial cells was substantiated by increased expression of activation markers (CD54 and CD105) and the LPS receptor, TLR4, on CD31-positive brain endothelial cells isolated by flow cytometry. Transcript analyses further revealed significant upregulation of Cxcl10, C3, Ccl2, Il1b, Cxcl2, and Cxcl1 in these activated endothelial cells, consistent with identification of MyD88 as a regulator of these transcripts by pathway analysis. Using conditional brain endothelial gene ablation strategies, we establish that MyD88-dependent endothelial TLR4 signaling and endothelial Cxcl10 expression are essential for LPS-induced neuroprotection and microglial activation. CXCL10 production by brain endothelial cells in response to circulating TLR ligands thus provides a pathway to directly or indirectly signal to CXCR3 on neurons and/or microglia. Targeting activation of brain endothelial receptors provides an attractive and practical approach for inducing transient neuroprotection.
2022-02-01 | GSE193015 | GEO
Project description:ARPCs Can Revert Lps-Induced Endothelial-to-Mesenchymal Transition of Endothelial Cells
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Project description:Phenotypic heterogeneity among arterial ECs is particularly relevant to atherosclerosis since the disease occurs predominantly in major arteries, which vary in their atherosusceptibility. To explore EC heterogeneity, we used DNA microarrays to compare gene expression profiles of freshly harvested porcine coronary and iliac artery ECs. We demonstrate that in vivo the endothelial transcriptional profile of a coronary artery (the right coronary artery) is intrinsically different from that of a major conduit vessel (the external iliac artery), and that this difference is consistent with former vessel being more prone to atherosclerosis. Keywords: coronary atherosclerosis, endothelial heterogeneity, microarray, gene expression Endothelial cells were freshly harvest from right coronary, left and right iliac arteries from four pigs. RNA were isolated and expression profiles were obtained using olig microarrays.
2010-06-20 | E-GEOD-10938 | biostudies-arrayexpress
Project description:The vascular endothelium may play a role in the response to infectious agents and in the pathophysiology of disease processes resulting in capillary leak such as septic shock and acute respiratory distress syndrome. In order to study the effect of endotoxin on endothelial cell function, human lung microvascular endothelial cells in culture were exposed to lipopolysaccharide (LPS), 10 ng, for 4, 8, or 24 hours and changes in mRNA expression were studied using Affymetrix HG U133plus2 gene arrays. A principal components analysis revealed that LPS treatment was the primary source of variability in the data. LPS treatment of endothelial cells for 4, 8, or 24 hours resulted in the upregulation by two-fold or greater of 275, 260 and 141 genes respectively. LPS treatment resulted in the down regulation by 50% or greater of 176, 263 and 79 genes at 4, 8, or 24 hours respectively. Up regulated genes at 4 or 8 hours were enriched in those encoding for cytokines, secreted proteins, cell membrane proteins and proteins controlling signal transduction and transcriptional regulation. Down regulated genes at each of the time points included those coding for cell membrane proteins, transcriptional regulation and metabolism. At each time point, a significant proportion of the genes identified as changed were unique to that time point. Experiment Overall Design: In order to study the effect of endotoxin on endothelial cell function, human lung microvascular endothelial cells in culture were exposed to lipopolysaccharide (LPS), 10 ng, for 4, 8, or 24 hours and changes in mRNA expression were studied using Affymetrix HG U133plus2 gene arrays. Controls for each time point with no LPS exposure were also run. An N of 4 for each time point and treatment was used.
2008-06-14 | E-GEOD-5883 | biostudies-arrayexpress
Project description:Analysis of gene expression in glioma-associated endothelial cells in Tie2-Cre,Pfn1fl/fl:Y129F and Pfn1fl/fl:Y129F mice We detected different gene expression patterns in the tumor-associated endothelial cells in Tie2-Cre,Pfn1fl/fl:Y129F and Pfn1fl/fl:Y129F mice
2014-02-25 | GSE55295 | GEO