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Gene expression profiling in mouse livers after administration of both hydrogen-rich water and hydrogen gas

ABSTRACT: Molecular hydrogen is a hopeful agent for oxidative stress-related and/or inflammatory disorders. However, the molecular mechanism for these therapeutic effects of hydrogen still remains to be fully elucidated. We examined whether molecular hydrogen alters gene expression levels in normal mouse livers by DNA microarray analysis. We identified 140 mouse genes that were upregulated (31 genes) or downregulated (109 genes) after three weeks of the inhalation of 2% hydrogen-containing air with oral intake of hydrogen-rich water. Ingenuity Pathway Analysis revealed that hydrogen influenced expression of NF-kB- and NFAT-regulated genes. Western blot analysis showed that hydrogen attenuated Erk, p38 MAPK, and NF-kB signaling in mouse livers.

ORGANISM(S): Mus musculus

PROVIDER: GSE48826 | GEO | 2014/08/01

SECONDARY ACCESSION(S): PRJNA211856

REPOSITORIES: GEO

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Gene expression profiling in mouse livers after administration of both hydrogen-rich water and hydrogen gas

Project description:Molecular hydrogen is a hopeful agent for oxidative stress-related and/or inflammatory disorders. However, the molecular mechanism for these therapeutic effects of hydrogen still remains to be fully elucidated. We examined whether molecular hydrogen alters gene expression levels in normal mouse livers by DNA microarray analysis. We identified 140 mouse genes that were upregulated (31 genes) or downregulated (109 genes) after three weeks of the inhalation of 2% hydrogen-containing air with oral intake of hydrogen-rich water. Ingenuity Pathway Analysis revealed that hydrogen influenced expression of NF-kB- and NFAT-regulated genes. Western blot analysis showed that hydrogen attenuated Erk, p38 MAPK, and NF-kB signaling in mouse livers. We divided 10-week male BALB/c mice into two groups: 1) control group: fed with control water in air (n=4), 2) hydrogen-treated group: fed with hydrogen-rich water in 2% hydrogen/98% air (n=4). Hydrogen-rich water (0.7mM dissolved hydrogen) was generated from distilled water with 0.44 mM Na2SO4 using Aquela Blue, a water-electrolyzing device to produce electrolyzed hydrogen-saturated water near neutral pH (MiZ Co., Ltd, Fujisawa, Japan). The control water was prepared by gently stirring hydrogen-rich water in open air for 24 hours. Hydrogen-rich water or control water was administrated ad libitum to the mice with a 50-ml closed glass vessel equipped with an outlet line having a ball bearing. After 3-week rearing, the mice were sacrificed and their livers were removed for RNA extraction. We mixed equal amount of RNA from four mice in each group (control vs. hydrogen-treated) and compared gene expression profile by microarray.

2014-08-01 | E-GEOD-48826 | biostudies-arrayexpress

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Project description:The effects of the administration of molecular hydrogen-saturated drinking water (hydrogen water) on hepatic gene expression were investigated in rats. Using DNA microarrays, 548 upregulated and 695 downregulated genes were detected in the liver after a 4-week administration of hydrogen water. Gene Ontology analysis revealed that genes for oxidoreduction-related proteins, including hydroxymethylglutaryl CoA reductase, were significantly enriched in the upregulated genes.

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2007-04-01 | GSE6747 | GEO

Requirement for NF-kB in maintenance of molecular and behavioral circadian rhythms in mice.

Project description:Purpose: In this study we employed unbiased, genome-wide techniques to investigate how inflammation-induced NF-kB activation by acute (LPS vs. saline) and chronic (high-fat diet vs. regular chow) environmental stimuli leads to circadian disruption. Methods: We performed ChIP-seq with antibodies directed against the p65 subunit of NF-kB, CLOCK, BMAL1, H3K27Ac and RNA Poll II in livers from mice treated with LPS or saline. ChIP-seq analysis was also performed in livers from mice that were fed high-fat diet for 4 weeks or regular chow. In addition, we performed ChIP-seq with BMAL1 in mouse embryonic fibroblast deficient in p65. Results: Induction of NF-kB reconfigures the genome-wide position of core clock transcription factors. Acute (i.e. LPS) and chronic (e.g. high-fat diet) inflammation-induced NF-kB re-localizes components of the forward limb of clock (CLOCK/BMAL1) to sites convergent with NF-kB and acetylated H3K27 and enriched in RNA POL II in liver. In addition, NF-kB activation leads to higher p65 binding specific to E-box elements within the negative limb of the clock with both acute and chronic stimuli. Conclusions: Our findings cast new light on NF-kB as a pivotal genomic control node integrating metabolic inflammation and circadian systems at both the cellular and organismal levels. In particular, NF-kB directly regulates the expression of the negative limb of the clock while at the same time the clock activator TFs CLOCK/BMAL1 co-localize with NF-kB at new sites to regulate transcription following inflammatory stimuli. In addition, our data indicate significant overlap between NF-kB activation following both acute and chronic inflammatory challenges in liver.

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2024-05-09 | PXD037534 | JPOST Repository

Mus musculus

Project description:NF-kB target genes in dendritic cells

| PRJNA100801 | ENA