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Hydrogen sulfide (H2S) modulates lifespan of C.elegans

ABSTRACT: 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.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE16975 | GEO | 2013/07/30

SECONDARY ACCESSION(S): PRJNA117271

REPOSITORIES: GEO

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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. The global transcriptome of control nematodes (raised using standardized laboratory conditions) was compared to nematodes exposed to 100 uM GYY4137 (morpholin-4-ium 4 methoxyphenyl(morpholino) phosphinodithioate), a slow releasing H2S donor drug.

2013-07-30 | E-GEOD-16975 | 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.

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The Global Transcriptional Response of Fission Yeast to Hydrogen Sulfide

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

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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.

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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.

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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.

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

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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

HIF-1 and SKN-1 Coordinate the Transcriptional Response to Hydrogen Sulfide in C. elegans

Project description:Hydrogen sulfide (H2S) has dramatic physiological effects on animals that are associated with improved survival in changing conditions. C. elegans grown in H2S are long-lived and thermotolerant (1). To begin to identify mechanisms by which adaptation to H2S effects fundamental physiological functions, we have defined transcriptional changes associated with the response to H2S. Using microarray analysis we observe rapid changes in the abundance of specific mRNAs. The number and magnitude of transcriptional changes increased with the duration of H2S exposure. Functional annotation suggests that genes associated with protein homeostasis are upregulated upon prolonged exposure to H2S. Previous work has shown that the hypoxia-inducible transcription factor, HIF-1, is required for survival in H2S (2). We show that hif-1 is required for all early transcriptional changes in H2S. However, our data suggest that other factors may also regulate transcriptional effects of H2S exposure, and we demonstrate that SKN-1, the C. elegans homologue of NRF2, is also required for some H2S-dependent changes in transcription. Moreover, we have found that, like hif-1, skn-1 is essential to survive exposure to H2S. Our results support a model in which HIF-1 and SKN-1 coordinate a broad transcriptional response to H2S, with the end result to affect a global reorganization of protein homeostasis networks. We propose that these transcriptional responses contribute to the effects of adaptation to H2S on lifespan and thermotolerance.

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