Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene profiling comparison between hydrogen sulfide- and N-methyl-D-aspartate-induced neuronal deaths

ABSTRACT: Hydrogen sulfide (H2S), present in abundance in the mammalian brain, has recently been demonstrated to induce a dose- and time-dependent apoptotic-necrotic continuum in murine primary cortical neurons, which was successfully attenuated upon application of N-methyl-D-aspartate (NMDA) receptor antagonist. The current study focused on gaining an insight into the molecular mechanisms of H2S–mediated neuronal death pertaining to NMDA receptors activation through global gene expression comparisons.

ORGANISM(S): Mus musculus

PROVIDER: GSE16035 | GEO | 2013/01/23

SECONDARY ACCESSION(S): PRJNA115395

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Global gene profiling comparison between hydrogen sulfide- and N-methyl-D-aspartate-induced neuronal deaths

Project description:Hydrogen sulfide (H2S), present in abundance in the mammalian brain, has recently been demonstrated to induce a dose- and time-dependent apoptotic-necrotic continuum in murine primary cortical neurons, which was successfully attenuated upon application of N-methyl-D-aspartate (NMDA) receptor antagonist. The current study focused on gaining an insight into the molecular mechanisms of H2S–mediated neuronal death pertaining to NMDA receptors activation through global gene expression comparisons. A total of 24 RNA samples were analyzed. There are 2 treatment conditions, namely 200uM sodium hydrosulfide and 200uM N-methyl-D-asparate. 3 replicates were collected for each of the selected time-points (5h, 15h and 24h), in addition to 6 replicates of shared vehicle control. The supplementary file 'GSE16035_non-normalized_data.txt' contains non-normalized data for Samples GSM401312-GSM401335.

2013-01-23 | E-GEOD-16035 | biostudies-arrayexpress

Transcriptomic study of hydrogen sulfide toxicity in Methylococcus capsulatus

Project description:Stress response of Methylococcus capsulatus str.Bath toward hydrogen sulfide (H2S) was investigated via physiological study and transcriptomic profiling. M. capsulatus (Bath) can grow and tolerate up to 0.75%vol H2S in headspace. Vast change in pH suggests biological relevant sulfide oxidation. Dozens of H2S-sensitive genes were identified from comparison of cell transcriptome in different H2S concentrations. Mc sulfide quinone reductase (SQR) and persulfide dioxygenase were found to be active during sulfide detoxification. Moreover, xoxF, a novel lanthanide(Ln)-dependent methanol dehydrogenase (MDH) was overexpressed in H2S while mxaF, a calcium-dependent MDH, was down-regulated, and such MDH switch phenomenon is also well known to be induced by addition of lanthanide via an as-yet-unknown mechanism. Activities in quorum sensing and RND efflux pump also suggest their role in sulfide detoxification, and might provide insight on the xoxF/mxaF switch mechanism.

2021-12-24 | GSE192351 | GEO

The Global Transcriptional Response of Fission Yeast to Hydrogen Sulfide

2012-06-15 | GSE30025 | GEO

Hydrogen sulfide (H2S) modulates lifespan of C.elegans

Project description:Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated.

2013-07-30 | GSE16975 | GEO

Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis

Project description:The ubiquitous gasotransmitter hydrogen sulfide (H2S) has been recognised to play a crucial role in human health. However, a role for host H2S in pathogenesis has not yet been demonstrated. Using cystathionine -lyase (CSE) deficient mice, we demonstrated an unexpected role of H2S in Mtb pathogenesis. We showed that Mtb-infected CSE-/- mice survive longer than wild-type mice, and support reduced pathology and lower bacterial burdens in the lung, spleen and liver. Similarly, in vitro Mtb infection of macrophages resulted in reduced colony forming units (CFUs) in CSE-/-cells. Chemical complementation of infected wild-type and CSE-/-macrophages using the slow H2S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H2S is the effector molecule regulating Mtb survival in macrophages. Furthermore, we demonstrate that CSE promotes an excessive innate immune response, suppresses the adaptive immune response and reduces circulating IL1β, IL-6, TNFα, and IFN-γ levels in response to Mtb infection. Notably, Mtb infected CSE-/- macrophages show increased flux through glycolysis and the pentose phosphate pathway thereby establishing a critical link between H2S and central metabolism. Our data suggest that excessive H2S produced by the infected wild type mice reduce HIF-1α levels, thereby suppressing glycolysis and production of IL-1β, IL-6 and IL-12, and increasing bacterial burden. Clinical relevance was demonstrated by the spatial distribution of H2S producing enzymes in human necrotic, non-necrotic and cavitary pulmonary TB lesions. In summary, CSE exacerbates TB pathogenesis by altering immunometabolism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB control.

2020-04-06 | GSE143619 | GEO

Hydrogen sulfide (H2S) modulates lifespan of C.elegans

2013-07-30 | E-GEOD-16975 | biostudies-arrayexpress

The Global Transcriptional Response of Fission Yeast to Hydrogen Sulfide

Project description:Hydrogen sulfide (H2S) as an important gasotransmitter has fundamental roles in human diseases. The cellular effect of H2S has received lots of attention recently. H2S can affect ion channels, transcription factors and kinase in mammals. The mechanism of cellular effect of H2S is not completely understood. We used fission yeast as a model organism to study the global transcriptional profile in response to H2S by microarray. The wild type S. pombe cells were grown in liquid medium to OD600=0.5. Then the cells were treated with or without 50M-NM-<M of NaHS (Sigma, St Louis, MO, USA) for 30 min at 30M-bM-^DM-^C.Total RNA was extracted from cells using a hot phenol method.The microarray experiments including RNA purification, cDNA probe preparation, hybridization, washing, scanning, image analysis, normalization and data processing were performed by Shanghai Biochip Co., Ltd. as described in the Affymetrix GeneChip_Expression Analysis Technical Manual. Three biological repeats were performed for the microarray experiments.

2012-06-14 | E-GEOD-30025 | biostudies-arrayexpress

Applying transcriptomics to screen the significantly altered genes, cell function and signal transduction pathway of chicken trachea exposured to hydrogen sulfide

Project description:Hydrogen sulfide (H2S) is well known to cause irritation and damage to airway following inhalation, but the mechanism by which H2S contributes to airway toxicity is unclear. We apply transcriptomics to demonstrate the possible effects, obtain valuable information about adverse health effects following H2S exposure and to study the molecular mechanisms of the gas toxicity in trachea.

2022-05-27 | GSE131820 | GEO

Applying of transcriptomics to screen the significantly altered genes, cell function and signal transduction pathway of chicken trachea exposed to hydrogen sulfide

2021-09-04 | GSE119429 | GEO

Hydrogen sulfide sensitizes Acinetobacter baumannii to killing by antibiotics.

Project description:The production of endogenous hydrogen sulfide (H2S) has been shown to confer antibiotic tolerance in all bacteria studied to date. Therefore, this mediator has been speculated to be a universal defense mechanism against antibiotics in bacteria. This is assuming that all bacteria produce endogenous H2S. In this study, we established that the pathogenic bacteria Acinetobacter baumannii does not produce endogenous H2S, giving us the opportunity to test the effect of exogenous H2S on antibiotic tolerance in a bacterium that does not produce it. By using a H2S-releasing compound to modulate the sulfide content in A. baumannii, we demonstrated that instead of conferring antibiotic tolerance, exogenous H2S sensitized A. baumannii to multiple antibiotic classes, and was able to revert acquired resistance to gentamicin. Exogenous H2S triggered a perturbation of redox and energy homeostasis that translated into hypersensitivity to antibiotic killing. We propose that H2S could be used as an antibiotic-potentiator and resistance-reversion agent in bacteria that do not produce it.

2021-06-08 | PXD020384 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data