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
2004-02-26 | GSE1042 | GEO
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
2004-02-26 | GSE1038 | GEO
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:Deregulated retinal angiogenesis directly cause vision loss in many ocular diseases, such as diabetic retinopathy and retinopathy of prematurity. To identify endothelial-specific genes expressed in angiogenic retinal vessels, we purified genetically labeled endothelial cells from Tie2-GFP transgenic mice and performed gene expression profiling using DNA microarray. To find out genes associated with angiogenesis, comparisons of microarray data were carried out between GFP-negative non-endothelial retinal cells and GFP-positive retinal endothelial cells in angiogenic P8 retina. Eighteen arrays are included. Utilizing fluorescence-activated cell sorting (FACS), we isolated endothelial cells as GFP-positive cells from P8 retina in homozygous Tie2-GFP transgenic mice. GFP-negative cells were served as non-endothelial control. RNA extracts from sorted cells were amplified and then hybridized to Affymetrix MGU74v2 series arrays in triplicate.
2011-04-17 | E-GEOD-27238 | biostudies-arrayexpress
Project description:Deregulated retinal angiogenesis directly cause vision loss in many ocular diseases, such as diabetic retinopathy and retinopathy of prematurity. To identify endothelial-specific genes expressed in angiogenic retinal vessels, we purified genetically labeled endothelial cells from Tie2-GFP transgenic mice and performed gene expression profiling using DNA microarray. To find out genes associated with angiogenesis, comparisons of microarray data were carried out between GFP-negative non-endothelial retinal cells and GFP-positive retinal endothelial cells in angiogenic P8 retina.
2011-04-17 | GSE27238 | GEO
Project description:The objective of this study is to create an encyclopedia of all genes expressed in the glomerular endothelial cell under normal and diabetic conditions. We utilized Tie2-GFP transgenic mice to mark cells of the glomerular endothelium. To induce diabetic nephropathy (DB), a genetic model of DB, BKS.Cg-m +/+ Leprdb/J from Jax laboratories was used. We utilized fluorescent activated cell sorting (FACS) to isolate glomerular endothelial cells from normal and diabetic mice. The RNAs from these samples were isolated and utilized to hybridize to microarrays, which offers a powerful, efficient and effective method for the creation of a gene expression atlas. Microarrays were used to identify the transciptional differences that occur in the glomular endothelium of a diabetic mouse. Diabetic and control mice carrying the Tie2-GFP transgenic were utilized to isolate the endothelial cells from the adult glomerulus. The endothelial cells were isolated from the glomerulus using FACS. RNA was isolated and the gene expression profiles were determined by microarrays.
2010-08-16 | E-GEOD-21324 | biostudies-arrayexpress
Project description:Background: Blood-retinal barrier cells are known to exhibit a massive phenotypic change during experimental autoimmune uveitis (EAU) development. In an attempt to investigate the mechanisms of blood-retinal barrier (BRB) breakdown at a global level, we studied the gene regulation of total retinal cells and retinal endothelial cells during non-infectious uveitis. Methods: Retinal endothelial cells were isolated by flow cytometry either in Tie2-GFP mice (CD31+ CD45- GFP+ cells), or in wild type C57BL/6 mice (CD31+ CD45- endoglin+ cells). EAU was induced in C57BL/6 mice by adoptive transfer of IRBP1-20-specific T cells. Total retinal cells and retinal endothelial cells from naïve and EAU mice were sorted and their gene expression compared by RNA-Seq. Protein expression of selected genes was validated by immunofluorescence on retinal wholemounts and cryosections and by flow cytometry. Results: Retinal endothelial cell sorting in wild type C57BL/6 mice was validated by comparative transcriptome analysis with retinal endothelial cells sorted from Tie2-GFP mice, which express GFP under the control of the endothelial-specific receptor tyrosine kinase promoter Tie2. RNA-Seq analysis of total retinal cells mainly brought to light upregulation of genes involved in antigen presentation and T cell activation during EAU. Specific transcriptome analysis of retinal endothelial cells allowed us to identify 82 genes modulated in retinal endothelial cells during EAU development. Protein expression of 5 of those genes (serpina3n, lipocalin 2, ackr1, lrg1 and lamc3) was validated at the level of inner BRB cells. Conclusion: Those data not only confirm the involvement of known pathogenic molecules but further provide a list of new candidate genes and pathways possibly implicated in inner BRB breakdown during non-infectious posterior uveitis.
2020-01-28 | GSE144168 | GEO
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