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Role of endothelial STING1 in the transcriptional response to LPS

ABSTRACT: RNA-seq analysis of kidney endothelium and whole kidney from mice 15 hours after an intraperitoneal challenge with 250 micrograms of LPS per mouse.

ORGANISM(S): Mus musculus

PROVIDER: GSE277816 | GEO | 2025/08/11

REPOSITORIES: GEO

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Role of endothelial SOCS3 in the transcriptional response to LPS

Project description:Translating affinity purification (TRAP)-mediated analysis of kidney endothelial translatome of bulk kidney RNA-seq from mice 15 hours after an intraperitoneal challenge with 250 micrograms of LPS per mouse.

2025-08-11 | GSE277696 | GEO

Cardiac endothelial in vivo responses to LPS

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

In vivo LPS effects on cardiac endothelial RNA-15K cDNA array

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

Compare RNA profile between LPS+CPN and LPS+CPN+GGOH treated peritoneal macrophages

2013-11-12 | GSE48646 | GEO

In vivo LPS effects on cardiac endothelial RNA-15K cDNA array

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

Role of endothelial STING1 in the transcriptional response to LPS

Project description:Role of endothelial STING1 in the transcriptional response to LPS

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ARPCs Can Revert Lps-Induced Endothelial-to-Mesenchymal Transition of Endothelial Cells

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

STAT1-dependent expression in kidney endothelium from mice challenged with LPS

Project description:STAT1-dependent expression in kidney endothelium from mice challenged with LPS

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Compare RNA profile between LPS+CPN and LPS+CPN+GGOH treated peritoneal macrophages

Project description:To find out genes regulated by geranylgeraniol (GGOH) treatment in peritoneal macrophage, we compared gene expression of cells treated with 200ng ml LPS and 250 micromolar compactin versus 200ng ml LPS, 250 micromolar compactin and 100micromolar GGOH. To find out upregulated or downregulated genes regulated by GGOH treatment in peritoneal macrophage (LPS+CPN treated cell).

2013-11-12 | E-GEOD-48646 | biostudies-arrayexpress

Control of LPS-response by DUSP1

Project description:Activation of the Mitogen activated protein kinase (MAPK) cascade following Toll-like receptor (TLR) stimulation enables innate immune cells to rapidly activate cytokine gene expression. A balanced response to signals of infectious danger requires that cellular activation is transient. Here, we identify the MAPK phosphatase Dual specificity phosphatase-1 (DUSP1) as an essential endogenous regulator of the inflammatory response to LPS. DUSP1-deficient (DUSP1-/-) bone marrow derived macrophages showed selectively prolonged activation of p38 MAPK and increased cytokine production. Intraperitoneal challenge of DUSP1-/- mice with LPS caused increased lethality and overshooting production of IL-6 and TNF?. Transcriptional profiling revealed that DUSP1 controls a significant fraction of LPS-induced genes, that includes IL-6 and IL-10 as well as the chemokines CCL3, CCL4 and CXCL2. In contrast, the expression of the important mediators of endotoxin lethality, IFN? and IL-12, was not significantly altered by the absence of DUSP1. These data together demonstrate a specific regulatory role of DUSP1 in controlling a subset of LPS-induced genes that determines the outcome of endotoxin shock. Keywords: in vivo analysis of splenic mRNA expression

2005-12-15 | GSE3565 | GEO

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