Molecular hydrogen modulates gene expression via histone modification and induces the mitochondrial unfolded protein response
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ABSTRACT:
PROVIDER: PRJNA399265 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-09-08 | GSE102913 | GEO
Project description:Characterization of post-translational modification of nitrogenase in Rhodopseudomonas palustris strains that produce hydrogen gas constitutively.
2012-03-15 | GSE32292 | GEO
Project description:How retinal pigmented epithelial (RPE) cells degenerate from oxidative stress in age-related macular degeneration (AMD) is incompletely understood. The study's intent was to identify key cytoprotective pathways activated by oxidative stress, and to determine the extent of their protection. Immunohistochemistry was used to identify the unfolded protein response (UPR) and mitochondria in the RPE of AMD samples. Maculas with early AMD had prominent IRE1α, but minimal mitochondrial TOM20 immunolabeling in mildly degenerated RPE. RPE cells treated with cigarette smoke extract (CSE), by microarray analysis, had over-represented genes involved in the antioxidant and unfolded protein response, and mitochondrial location. CSE induced the UPR sensors IRE1α, p-PERK, and ATP6, which activated CHOP. CHOP knockdown compromised cell viability after CSE exposure. At the same CSE doses, mitochondria generated superoxide anion and produced less ATP. In mice given intravitreal CSE, the RPE had increased IRE1α and decreased ATP, which elicited RPE epithelial-mesenchymal transition, as suggested by altered ZO1 immunolabeling of RPE flatmounts. Our experiments indicate that RPE cells exposed to oxidative stress respond with a cytoprotective antioxidant and unfolded protein response, but develop mitochondrial impairment that contributed to epithelial mesenchymal transition. With similar responses in the RPE of early AMD samples, these results suggest that mitochondria are vulnerable to oxidative stress while the ER elicits a protective response during early AMD. A total of 9 samples were analyzed: 3 control samples, 3 samples treated with 100ug/ml of Cigarette Smoke Condensate, and 3 samples treated with 250ug/ml of Cigarettes Smoke Condensate.
2014-01-30 | E-GEOD-49107 | biostudies-arrayexpress
Project description:We have previously demonstrated that molecular hydrogen (H2) neutralizes hydroxyl radical (•OH) in cultured-cells and protects cells and tissues against oxidative stress. Growing evidence has confirmed that H2-consumption exhibits preventive and therapeutic effects in patients with various diseases as well as model animals. Moreover, a small amount of H2 modulates signal transduction for regulating the expression of various genes; however, the primary target of H2 for exhibiting a variety of phenotypes was completely unknown. Here we show that H2 at low amounts manipulates oxidized phospholipid mediators to modulate Ca2+-signal transduction and gene expression.
2014-10-17 | GSE62434 | GEO
Project description:We have previously demonstrated that molecular hydrogen (H2) neutralizes hydroxyl radical (M-bM-^@M-"OH) in cultured-cells and protects cells and tissues against oxidative stress. Growing evidence has confirmed that H2-consumption exhibits preventive and therapeutic effects in patients with various diseases as well as model animals. Moreover, a small amount of H2 modulates signal transduction for regulating the expression of various genes; however, the primary target of H2 for exhibiting a variety of phenotypes was completely unknown. Here we show that H2 at low amounts manipulates oxidized phospholipid mediators to modulate Ca2+-signal transduction and gene expression. Gene expression was measured at 4 hours after exposure to phospholipid, PAPC or oxidized PAPC that had been air-oxidized for 3 days with 0, 1.3 or 5% H2. Three independent experiments were performed for each experiment.
2014-10-17 | E-GEOD-62434 | biostudies-arrayexpress
Project description:How retinal pigmented epithelial (RPE) cells degenerate from oxidative stress in age-related macular degeneration (AMD) is incompletely understood. The study's intent was to identify key cytoprotective pathways activated by oxidative stress, and to determine the extent of their protection. Immunohistochemistry was used to identify the unfolded protein response (UPR) and mitochondria in the RPE of AMD samples. Maculas with early AMD had prominent IRE1α, but minimal mitochondrial TOM20 immunolabeling in mildly degenerated RPE. RPE cells treated with cigarette smoke extract (CSE), by microarray analysis, had over-represented genes involved in the antioxidant and unfolded protein response, and mitochondrial location. CSE induced the UPR sensors IRE1α, p-PERK, and ATP6, which activated CHOP. CHOP knockdown compromised cell viability after CSE exposure. At the same CSE doses, mitochondria generated superoxide anion and produced less ATP. In mice given intravitreal CSE, the RPE had increased IRE1α and decreased ATP, which elicited RPE epithelial-mesenchymal transition, as suggested by altered ZO1 immunolabeling of RPE flatmounts. Our experiments indicate that RPE cells exposed to oxidative stress respond with a cytoprotective antioxidant and unfolded protein response, but develop mitochondrial impairment that contributed to epithelial mesenchymal transition. With similar responses in the RPE of early AMD samples, these results suggest that mitochondria are vulnerable to oxidative stress while the ER elicits a protective response during early AMD.
2014-01-30 | GSE49107 | GEO
Project description:Characterization of post-translational modification of nitrogenase in Rhodopseudomonas palustris strains that produce hydrogen gas constitutively. To characterize the effect of yeast extract as nitrogen source on gene expression under nitrogen fixing conditions, expression profiles of wild-type cells grown on either NF plus yeast extract and succinate and PM plus ammonium sulfate and succinate were compared using Affymetrix GeneChip. Using NF plus yeast extract and succinate media, transcriptome profiles of various mutants and wild-type cells were compared using glass spotted microarrays.
2012-03-15 | E-GEOD-32292 | biostudies-arrayexpress
Project description:We show that mitochondrial aconitase, ACO-2, a Krebs cycle enzyme that catalyzes the conversion of citrate to isocitrate, inhibits immunity against pathogenic bacteria in C. elegans. We found that genetic inhibition of aco-2 enhanced mitochondrial unfolded protein response, subsequently upregulating ATFS-1 transcription factor, which contributed to enhanced immunity against pathogenic bacteria.
2023-06-01 | GSE181546 | GEO
Project description:The relationship between oxidative stress and cardiac stiffness is thought to involve modifications to the giant muscle protein titin, which in turn can determine the progression of heart disease. In vitro studies have shown that S-glutathionylation and disulfide bonding of titin fragments could alter the elastic properties of titin; however, whether and where titin becomes oxidized in vivo is less certain. Here we demonstrate, using multiple models of oxidative stress in conjunction with mechanical loading, that immunoglobulin domains preferentially from the distal titin spring region become oxidized in vivo through the mechanism of unfolded domain oxidation (UnDOx). Via oxidation type-specific modification of titin, UnDOx modulates human cardiomyocyte passive force bidirectionally. UnDOx also enhances titin phosphorylation and, importantly, promotes non-constitutive folding and aggregation of unfolded domains. We propose a mechanism whereby UnDOx enables the controlled homotypic interactions within the distal titin spring to stabilize this segment and regulate myocardial passive stiffness.
2020-09-15 | PXD018174 | Pride
Project description:N6-methyladenosine (m6A) is the most common prevalent internal modifications found in many of the eukaryotic mRNA and plays an important role in RNA metabolism including pre-mRNA processing, mRNA stability, RNA splicing, RNA export and nuclear retention. Serrate is a component of the Dicer complex, plays as a key factor in RNA metabolism. We here reported SERRATE acts as a key regulator of mRNA m6A modification in Arabidopsis. Loss function of SE results in significant global m6A level reduction in the se-1 mutant comparing to the Col-0. SE positively regulates the transcription of MTA and MTB. In addition, SE physically interacts and functionally works with the m6A writer complex MTA and MTB which affects the binding of m6A methylase to mRNA. Taking together, our data provides a molecular framework that SE modulates m6A mRNA modification in Arabidopsis.
2023-11-01 | GSE241248 | GEO