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Expression in Kir6.1-deficient heart following LPS challenge

ABSTRACT: KATP opposes depolarization of cells in the heart, smooth muscle, and other tissues by permitting the efflux of potassium ions and this efflux is evidently required to prevent unopposed vasoconstriction and insufficiency of coronary artery blood flow triggered by one or more cytokines induced in response to LPS. The cytokine(s) involved must elicit a dysfunctional response in the Kir6.1-deficient environment, and to gain further insight into the effects of the mutation, we examined the transcriptional status of whole heart, isolated from normal C57BL/6J mice or KcnJ8Md/Md mice, before and after injection of 1 μg of LPS Keywords: Time course, stress response, disease state analysis, genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE7605 | GEO | 2007/11/01

SECONDARY ACCESSION(S): PRJNA100169

REPOSITORIES: GEO

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Transcription profiling of mouse Kir6.1-deficient heart following LPS challenge

Project description:KATP opposes depolarization of cells in the heart, smooth muscle, and other tissues by permitting the efflux of potassium ions and this efflux is evidently required to prevent unopposed vasoconstriction and insufficiency of coronary artery blood flow triggered by one or more cytokines induced in response to LPS. The cytokine(s) involved must elicit a dysfunctional response in the Kir6.1-deficient environment, and to gain further insight into the effects of the mutation, we examined the transcriptional status of whole heart, isolated from normal C57BL/6J mice or KcnJ8Md/Md mice, before and after injection of 1 Î¼g of LPS Experiment Overall Design: 3 mice per genotype were injected with 0.5 ug LPS in PBS or with PBS alone and hearts were collected after 30 min or 3 h.

2008-06-15 | E-GEOD-7605 | biostudies-arrayexpress

Sphingobium Nickel resistance analysis by RNA-seq approach

Project description:Nickel is an essential component of many eukaryotic and prokaryotic metallo-enzymes. Due to its employment in many industrial applications, wastewaters from industrial plants often contain millimolar concentrations of Ni2+ that are toxic and life-threatening for many organism. Several lines of preliminary evidence suggest that members of the genus Sphingobium are able to grow in the presence of high concentrations of metal ions. We have isolated a novel Sphingobium strain (sp. ba1) able to grow in the presence of high concentrations (up to 20 mM) of NiCl2. Sequencing of its genome allowed the identification of several genes coding for proteins potentially involved in efflux-mediated resistance mechanisms. Here we use the RNA-seq approach to analyze the response of the Sphingobium sp. ba1 strain to high concentrations (10 mM) of Ni ions. Transcriptomic data show the differential expression of about one-hundred and twenty genes, most of which are up-regulated and encode proteins such as membrane proteins and components of metal efflux systems, enzymes involved in oxidative stress responses (catalases, peroxidases) and signal transduction systems.

2017-07-03 | E-MTAB-5828 | biostudies-arrayexpress

Investigating B cell stimulation in ubiquilin-1 KO mice

Project description:Ubiquilins are a family of proteins involved in proteasomal degradation of mislocalized membrane proteins. Here, Greer et al. demonstrate that Ubqln1 is required for BCR-driven B cell proliferation through maintenance of protein synthesis following stimulation. In the absence of Ubqln1, mitochondrial proteins accumulate in the cytosol, which may account for the observed proteostasis. BCR stimulation of murine B cells induced a long-lasting mitochondrial depolarization that did not occur in response to LPS. We hypothesize that in the absence of Ubqln1, mitochondrial depolarization leads to an accumulation of mitochondrial membrane proteins in the cytosol, which leads to translational inhibition and a cell cycle block.

2017-11-01 | GSE86113 | GEO

Parallel kinase pathways stimulate actin polymerization at depolarized mitochondria

Project description:Mitochondrial damage (MtD) represents a dramatic change in cellular homeostasis, necessitating metabolic changes and stimulating mitophagy. One rapid response to MtD is rapid peri-mitochondrial actin polymerization, termed ADA (acute damage-induced actin). The activation mechanism for ADA is unknown. Here, we use mitochondrial depolarization or the complex I inhibitor metformin to induce ADA. We show that two parallel signaling pathways are required for ADA. In one pathway, increased cytosolic calcium activates in turn PKC-β, Rac, WAVE regulatory complex, and Arp2/3 complex. In the other pathway, a drop in cellular ATP activates in turn AMPK (through LKB1), Cdc42, and FMNL formins. We also identify putative guanine nucleotide exchange factors for Rac and Cdc42, Trio and Fgd1 respectively, whose phosphorylation states increase upon mitochondrial depolarization and whose suppression inhibits ADA. The depolarization-induced calcium increase is dependent on the mitochondrial sodium-calcium exchanger NCLX, suggesting initial mitochondrial calcium efflux. We also show that ADA inhibition results in enhanced mitochondrial shape changes upon mitochondrial depolarization, suggesting that ADA inhibits these shape changes. These depolarization-induced shape changes are not fragmentation but a circularization of the inner mitochondrial membrane, dependent on the inner mitochondrial membrane protease Oma1. ADA inhibition increases proteolytic processing of an Oma1 substrate, the dynamin GTPase Opa1. These results show that ADA requires the combined action of Arp2/3 complex and formin proteins to polymerize a network of actin filaments around mitochondria, and that the ADA network inhibits the rapid mitochondrial shape changes that occur upon mitochondrial depolarization.

2022-03-15 | PXD031699 | Pride

Epigenome-wide profiling uncovers novel pathway networks in human pulmonary arterial hypertension [pul36]

Project description:Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease that culminates in right heart failure. Vascular pathology in PH is characterized by pulmonary vasoconstriction and progressive vascular remodeling processes that affects all layers of the vascular wall (intima, media and adventitia).

2022-06-09 | GSE194080 | GEO

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

Project description:Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

2021-09-15 | GSE124083 | GEO

Genomic instability in the naturally and prematurely aged myocardium [RNA-Seq]

2021-09-15 | GSE124005 | GEO

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 2]

2021-09-15 | GSE129278 | GEO

Xijiao Dihuang decoction protects against sepsis-induced cardiac dysfunction

Project description:The goals of this study is to identify the differential expressed genes in heart of C57BL/6 mice with or without LPS treatment, and compare the differential expressed genes in the heart of LPS injection C57BL/6 mice after Xijiao Dihuang decoction(XJDHT) treatment. Briefly, the mice were randomly divided into 3 groups: control, LPS and LPS + XJDHT groups (n=4 for each group). Mice in Control and LPS groups were intraperitoneal injection with saline and 10mg/kg of LPS respectively, and orally administrated with saline; the mice in LPS + XJDHT groups were intraperitoneal injection with LPS (10 mg/kg) and orally administrated with 50 mg/kg /day of XJDHT for total 3 days. Then the heart were used to identify differentially expressed genes among different groups.

2022-10-24 | GSE215955 | GEO

Cellular Response of the bacterium Cupriavidus metallidurans CH34 to Strontium: bio-precipitation as strontium carbonate.

Project description:The physiological and transcriptomic response of the metal resistant bacterium Cupriavidus metallidurans strain CH34 in response to stable (non-radioactive) strontium ions (Sr) was investigated. C. metallidurans CH34 could survive and proliferate in the presence of relatively high concentrations of SrCl2 (D10 is 70mM, MIC is 120 mM). Precipitation of Sr as strontium carbonate was observed in the culture during aerobic growth of CH34 in the presence of 60 mM SrCl2. To identify the cellular mechanisms involved in the bioprecipitation process, gene expression in the cells was analyzed after short-time (30 min) exposure to low (5 mM) and high (60 mM) concentrations of SrCl2. The transcription of the gene clusters annotated as hmyFCBA and czcCBADRS, coding for ion efflux pumps, was significantly induced following exposure to Sr, and not with Ca. There were also significant changes is the transcription of the genes encoding TctCBA proteins involved in citrate uptake and two hypothetical porin coding genes following exposure Sr and Ca. These results highlight a specific molecular response of bacterium Cupriavidus metallidurans CH34 to Sr, including the identification of putative Sr specific efflux pumps, and thus the potential of this bacterium to distinguish Sr from Ca. These findings will help to better understand natural Sr (and Ca) microbial weathering or mineralization processes in the environment, and could be of interest for bioremediation or bioprocessing of (radioactive) Sr-containing water, soil or waste. Two-condition experiments. Comparing samples after induction with metals (Sr, Ca) versus non-induced samples. Biological triplicate. Each array contains 3 technical replicates.

2012-06-06 | E-GEOD-29863 | biostudies-arrayexpress

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