Transcriptome profiling of GLUTag cells with NaHS and GSH treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE220935 | GEO | 2024/05/06
REPOSITORIES: GEO
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Project description:Hydrogen sulfide (H2S), a traditionally known cytotoxic gas, has been recently included in the gasotransmitters family. Previous studies demonstrated that lifelong treatment with a slow H2S releasing donor extends yeast chronological lifespan (CLS), but it is not clear when the action of H2S benefits to CLS during yeast growth. Therefore, we investigated the effects of short H2S treatments at different time during yeast cell growth in the lifespan extension by using NaHS, a fast H2S-releasing donor. We show that short NaHS treatments at 4 days after inoculation extend yeast CLS while NaHS treatments earlier than 3 days after inoculation fail to do so. To reveal the mechanism of different consequences on yeast CLS of NaHS treatments at different times, we analyzed the transcriptome of Saccharomyces cerevisiae strain BY4742 with or without the early and late NaHS treatments. We found that the early and late NaHS treatments had similar effects on the expression of genes involved in pathways which are related to CLS regulation. Follow up qPCR and ROS analyses suggest that altered expression of some antioxidant genes by the early NaHS treatments were not stable enough to benefit CLS. Moreover, transcriptome data also indicated that some genes were regulated differently by the early and late H2S treatment such as genes involved in cell wall integrity. Specifically, we found that the expression of YPK2, a human SGK2 homolog and also a key regulator of the yeast cell wall synthesis, was significantly altered by the late NaHS treatment but not altered by the early NaHS treatment. Finally, the key role of YPK2 in CLS regulation by H2S is revealed by CLS data showing that the late NaHS treatment did not enhance the CLS of a ypk2 knockout mutant. This study sheds light on the molecular mechanism of CLS extension induced by H2S, and for the first time addresses the importance of H2S treatment timing for lifespan extension.
2023-10-02 | GSE160162 | GEO
Project description:Purpose: Hepatic stellate cell (HSC) and Hydrogen sulfide (H2S) both play important roles in Hepatocellar carcinoma (HCC). Whereas, in the microenvironment of HCC, whether HSC participates in regulating the biological process of HCC cells by releasing H2S remains elusive. In this study, we investigate how activated HSC influence HCC fate. Methods: The effects of LX-2 and H2S on biological functions of HCC cells were analyzed with Flow cytometry and CCK-8. RNA-sequencing, Western blotting, Quantitative real-time reverse transcription PCR (RT-qPCR), siRNA, immunofluorescence and chromatin immunoprecipitation (ChIP) assays were carried out to examine the effect of H2S on JNK/JunB-TNFSF14 (tumor necrosis factor superfamily member 14) signaling pathway. Specimens from HCC patients were analyzed by using RT-qPCR and Western blotting assays for evaluating the expression of TNFSF14. Statistical analysis was used to analyze the correlation between TNFSF14 expression and clinical data of HCC patients. Results: LX-2 cells is able to induce HepG2 and PLC/PRF/5 cells apoptosis by releasing H2S. RNA- sequencing results showed that TNFSF14 gene was changed in both LX-2 and NaHS group. NaHS dosage and time-dependently up-regulated TNFSF14 mRNA and protein expression in both HepG2 and PLC/PRF/5 cells. NaHS treated in HCC cells led to JNK/JunB signaling pathway activating and greater binding of JunB to its responsive elements on TNFSF14 promoter. Impairment of TNFSF14 induction alleviated LX-2 and NaHS induced apoptosis of HepG2 and PLC/PRF/5 cells. Furthermore, mRNA and protein expressions of TNFSF14 in HCC tissues was lower than in the adjacent tissue. HCC patients with low expression of TNFSF14 have higher malignant degree and poor prognosis. Conclusions: Demonstration of the involvement of HSC-derived H2S in JNK/JunB mediated expression of TNFSF14 gene strongly indicates H2S palys an important role in the regulation of HCC apoptosis.
2022-03-22 | GSE193660 | GEO
Project description:The essential thiol antioxidant, glutathione (GSH) is recruited into the nucleus of mammalian cells early in cell proliferation, suggesting a key role of the nuclear thiol pool in cell cycle regulation. However, the functions of nuclear GSH (GSHn) and its integration with the cytoplasmic GSH (GSHc) pools in whole cell redox homeostasis and signaling are unknown. Here we show that GSH is recruited into the nucleus early in cell proliferation in Arabidopsis thaliana, confirming the requirement for localization of GSH in the nucleus as a universal feature of cell cycle regulation. GSH accumulation in the nucleus was triggered by treatments that synchronize cells at G1/S as identified by flow cytometry and marker transcripts. Significant decreases in transcripts associated with oxidative signaling and stress tolerance occurred when GSH was localized in the nucleus. Increases in GSH1 and GSH2 transcripts accompanied the large increase in total cellular GSH observed during cell proliferation, but only GSH2 was differentially expressed in cells with high GSHn relative to those with an even intracellular distribution of GSH. Of the 7 Bcl-2 associated (BAG) genes in A. thaliana, only the nuclear-localized BAG 6 was differentially expressed in cells with high GSHn compared to GSHc. We conclude that GSHn is associated with decreased oxidative signaling and stress responses and that whole cell redox homeostasis is restored as the cell cycle progresses by enhanced GSH synthesis and accumulation in the cytoplasm. Arabidopsis cells were harvested at points during cell proliferation where GSH was localized either in the nucleus (GSHn) or where GSH was distributed throughout the cytoplasm (GSHc) for RNA extraction and hybridization on Affymetrix microarrays. We selected three stages where the GSH was into the nucleus and three stages where the GSH was distributed throughout the cells.
2010-02-27 | E-GEOD-20454 | biostudies-arrayexpress
Project description:Glutathione is a tripeptide involved in diverse aspects of plant metabolism. We investigated how the reduced form of glutathione, GSH, applied site-specifically to plants, affects zinc (Zn) distribution and behavior in oilseed rape plants (Brassica napus) cultured hydroponically. Foliar-applied GSH significantly increased the Zn content in shoots and the root-to-shoot Zn translocation ratio; furthermore, this treatment raised the Zn concentration in the cytosol of root cells and substantially enhanced Zn xylem loading. Notably, microarray analysis revealed that the gene encoding pectin methylesterase was upregulated in roots following foliar GSH treatment. We conclude that certain physiological signals triggered in response to foliar-applied GSH were transported via sieve tubes and functioned in root cells, which, in turn, increased Zn availability in roots by releasing Zn from their cell wall. Consequently, root-to-shoot translocation of Zn was activated and Zn accumulation in the shoot was markedly increased.
2019-05-29 | GSE109282 | GEO
Project description:The essential thiol antioxidant, glutathione (GSH) is recruited into the nucleus of mammalian cells early in cell proliferation, suggesting a key role of the nuclear thiol pool in cell cycle regulation. However, the functions of nuclear GSH (GSHn) and its integration with the cytoplasmic GSH (GSHc) pools in whole cell redox homeostasis and signaling are unknown. Here we show that GSH is recruited into the nucleus early in cell proliferation in Arabidopsis thaliana, confirming the requirement for localization of GSH in the nucleus as a universal feature of cell cycle regulation. GSH accumulation in the nucleus was triggered by treatments that synchronize cells at G1/S as identified by flow cytometry and marker transcripts. Significant decreases in transcripts associated with oxidative signaling and stress tolerance occurred when GSH was localized in the nucleus. Increases in GSH1 and GSH2 transcripts accompanied the large increase in total cellular GSH observed during cell proliferation, but only GSH2 was differentially expressed in cells with high GSHn relative to those with an even intracellular distribution of GSH. Of the 7 Bcl-2 associated (BAG) genes in A. thaliana, only the nuclear-localized BAG 6 was differentially expressed in cells with high GSHn compared to GSHc. We conclude that GSHn is associated with decreased oxidative signaling and stress responses and that whole cell redox homeostasis is restored as the cell cycle progresses by enhanced GSH synthesis and accumulation in the cytoplasm.
2010-02-22 | GSE20454 | GEO
Project description:It has been suggested that hydrogen sulfide (H2S) may play a pivotal role in mediating some of these caloric restriction (CR)-associated benefits. We therefore explored whether a novel slow-releasing H2S donor compound, FW1256, mimics CR and reproduces CR-associated effects in normal feeding Caenorhabditis elegans. Using transcriptomics analysis via RNA sequencing, we determined sets of differentially expressed genes (DEG) for FW1256-exposed wild-type C. elegans and eat-2 mutants, a genetic model of CR in C. elegans, relative to unexposed wild-type C. elegans. We found that, while FW1256 affects some of the same downstream genes as eat-2 mutation, global gene expression changes are dissimilar between FW1256-exposed C. elegans and eat-2 mutants, suggesting that novel slow-releasing H2S donor compound, FW1256, does not mimic CR at the transcriptional level.
2020-03-06 | GSE146412 | GEO
Project description:Murine or human cancer cells have high glutathione levels. Depletion of the elevated GSH inhibits proliferation of cancer cells. Molecular basis for this observation is little understood. In an attempt to find out the underlying mechanism, we reproduced these effects in transformed C3H10T1/2 and BALB/c 3T3 cells using diethyl maleate and studied cytogenomic changes in the whole mouse genome using spotted 8 M-CM-^W 60K arrays. Transformed cells revealed an increase in GSH levels. GSH depletion by DEM inhibited the growth of transformed cells. The non-cytotoxic dose of DEM (0.25 mM) resulted in GSH depletion, ROS generation, cell cycle arrest, apoptosis, decrease in anchorage independent growth, gene expression changes and activation of all three members of the MAPK family. Increase in intracellular GSH levels by GSHe countered the effect of DEM. These results support the physiological importance of GSH in regulation of gene expression for transformed cell growth restraint. This study is of interest in not only understanding the molecular biology of the transformed cells, but also in identifying new targets for development of gene therapy together with the chemotherapy. Agilent one-color experiment; Organism: Mus musculus; Agilent Custom Mouse Whole Genome Mouse 8x60k gene expression designed by Genotypic Technology Private Limited; Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442).
2014-06-02 | E-GEOD-44650 | biostudies-arrayexpress
Project description:To investigate the role of H2S in Chronic obstructive pulmonary disease (COPD), a rat model of COPD was established by cigarette smoking (CS) and intratracheal instillation of lipopolysaccharide (LPS). Rats were randomly divided into 4 groups: Control, CS+LPS, CS+LPS+NaHS and CS+LPS+propargylglycine (PPG). Transcription profiling of lung tissue comparing Control with CS+LPS, CS+LPS with CS+LPS+NaHS, and CS+LPS with CS+LPS+PPG. The goal was to determine the impact of H2S on gene expression profiling in rat model of COPD.
2021-09-24 | GSE184693 | GEO
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
Project description:JS-K, a NO donor which capable to induce cancer apopotosis, it's killing mechanism was investigated in this study. We found out that JS-K induce apopotosis via deregulating the GSH/GSSG redox couple.
2012-11-17 | GSE42344 | GEO