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Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

ABSTRACT: Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

PROVIDER: PRJNA541987 | ENA |

REPOSITORIES: ENA

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Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

Project description:Hypoxic pulmonary vasoconstriction (HPV) optimizes the match between ventilation and perfusion in the lung by reducing blood flow to poorly ventilated regions. Sepsis and endotoxemia impair HPV. We previously showed that nitric oxide synthase 2 (NOS2) is required, but not sufficient, for the effect of endotoxin on HPV. The aim of the current study was to identify additional factors that might contribute to the impairment of HPV during endotoxemia. Microarray gene expression profiling was determined using pulmonary tissues from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin (LPS) or saline challenge (control).

2019-05-09 | GSE130936 | GEO

Mouse kidney after systemic endotoxin challenge

Project description:8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest At t=0hr, mice had normal baseline renal function. At t=18hr, mice exhibited early renal injury, At t=42hr, mice had either recovered normal renal function or had persistent renal injury. We collected kidneys from 3 mice per time point. For the 42 hr time point, we collected kidneys from 3 mice with recovered renal function and kidneys from 3 mice with persistent renal injury. Mouse kidneys selected at successive stages of renal injury and recovery following systemic LPS challenge and volume resuscitation following LPS challenge.

2011-07-12 | E-GEOD-30576 | biostudies-arrayexpress

Mouse kidney after systemic endotoxin challenge

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Neural transcriptomic responses to endotoxin challenge across social treatments

Project description:The aim of this experiment was to test whether the social setting changed neural transcriptomic responses to an endotoxin challenge in zebra finches

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Gene expression Profiling of Peripheral Blood Leukocytes after Endotoxin Challenge in Humans

Project description:Peripheral blood mononuclear cells were isolated 0, 30 min, 6 h, 24 h, and 7 day after intravenous endotoxin challenge. Keywords: time course

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Neural transcriptomic responses to endotoxin challenge across social treatments

Project description:Neural transcriptomic responses to endotoxin challenge across social treatments

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IL-10 prevents pathological microglia hyperactivation following peripheral endotoxin challenge

Project description:Microglia, the resident macrophages of the brain parenchyma, are central players in CNS development, homeostasis and disorders. Distinct brain pathologies seem associated with discrete microglia activation modules. How microglia regain their ground state following challenges remains much less understood. Here, we explored the role of the IL-10 axis in restoring murine microglia homeostasis following peripheral endotoxin challenge. Specifically, we show that lipopolysaccharide (LPS)-challenged mice harboring IL-10 receptor-deficient microglia display neuronal impairment and succumb to fatal sickness. Addition of a microglial TNF deficiency rescues these animals, suggesting a microglia-based circuit driving pathology. Single cell transcriptome analysis revealed various IL-10 producing resident and recruited immune cell in the CNS, including most prominently Ly49D+ NK cells and neutrophils, but not microglia. Collectively, we define the kinetics of the microglia response to peripheral endotoxin challenge, including their activation and robust silencing, and highlight the critical role of non-microglial IL-10 in preventing deleterious microglia hyperactivation.

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IL-10 prevents pathological microglia hyperactivation following peripheral endotoxin challenge

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Ptch1+/- Nos2-/- medulloblastomas

Project description:This SuperSeries is composed of the following subset Series: GSE29192: Implication of Nos2 inactivation on the transcriptome of developing cerebellum and Ptch1+/- medulloblastomas (mRNA) GSE29199: Implication of Nos2 inactivation on genomic changes in Ptch1+/- medulloblastomas (array-CGH) Refer to individual Series

2011-12-01 | E-GEOD-29201 | biostudies-arrayexpress

Implication of Nos2 inactivation on the transcriptome of developing cerebellum and Ptch1+/- medulloblastomas (mRNA)

Project description:The Ptch1+/- strain constitues an established mouse model for the Shh-driven type of medulloblastoma. Combined Ptch1+/- Nos2-/- mice show a two-fold increased incidence for this tumor. Here, the impact of Nos2 inactivation on medulloblastoma development was investigated by gene expression profiling of tumor samples as well as healthy cerebellum at different ages and genotypes. Medulloblastoma samples from three Ptch1+/- and six combined Ptch1+/- Nos2-/- mice were analyzed. Healthy cerebellum taken from mice at postnatal day nine, six weeks after birth, and about 1 year of age were analyzed for wildtype animals and the genotypes Ptch1+/-, Ptch1+/- Nos2-/-, and Nos2-/-. The cerebellar developmental stages at six weeks and one year were measured in three biological replicates, while samples taken at postnatal day six consisted of pooled individual specimen. These were measured in three replicates being amplified and labelled in separate reactions. All samples were subjected to two-color hybridizations against Universal Reference RNA (Stratagene) with color-switch experiments yielding two technical replicates, respectively.

2011-12-01 | E-GEOD-29192 | biostudies-arrayexpress

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