TP53 modulates oxidative stress in Gata1+ erythroid cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE92754 | GEO | 2017/02/15
SECONDARY ACCESSION(S): PRJNA358512
REPOSITORIES: GEO
Similar Datasets
Project description:TP53 modulates oxidative stress in Gata1+ erythroid cells
| PRJNA358512 | ENA
Project description:Male germ cells from young and aged Rats were Isolated and cultured and then treated with pro-oxidant SIN-1 and antioxidant EUK134 Study of the response of isolated male germ cells from young and aged Brown Norway Rats to oxidative stress. Treatment of Isolated and cultured germ cells with pro-oxidant and antioxidant.
2015-04-30 | E-GEOD-66976 | biostudies-arrayexpress
Project description:Disruption of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how nearly lethal stresses affect circadian clocks. We found that near-lethal doses of reactive oxygen species (ROS)-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) M-bM-^@M-^Smediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-orchestrated crosstalk between the circadian, HSR, NFM-NM-:B-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in ROS-inducible disorders, various diseases, and death. Gene expression was measured 4h, 20h and 32h after treatment with 5 mM H2O2 for 10 min.
2013-11-09 | E-GEOD-47955 | biostudies-arrayexpress
Project description:It is well appreciated that reactive oxygen species (ROS) are deleterious to mammals, including humans, especially when generated in abnormally large quantities from cellular metabolism. Whereas the mechanisms leading to the production of ROS are rather well delineated, the mechanisms underlying tissue susceptibility or tolerance to oxidant stress remain elusive. Through an experimental selection over many generations, we have previously generated Drosophila melanogaster flies that tolerate tremendous oxidant stress and have shown that the family of antimicrobial peptides (AMP) is over-represented in these tolerant flies. Furthermore, we have also demonstrated that overexpression of even one AMP at a time (e.g. Diptericin) allows wild type flies to survive much better in hyperoxia. In the current study, we used a number of experimental approaches to investigate the potential mechanisms underlying hyperoxia tolerance in flies with antimicrobial peptide overexpression. We demonstrate that flies with Diptericin overexpression resist oxidative stress by increasing antioxidant enzyme activities and preventing an increase in ROS level after hyperoxia. Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirming that enhanced survival observed in these flies is related to improved redox homeostasis. We conclude that a) AMPs play an important role in tolerance to oxidant stress; b) overexpression of Diptericin changes the cellular redox balance between oxidant and antioxidant, and c) this change in redox balance plays an important role in survival in hyperoxia. Expression profiles of Drosophila melanogaster with anti-microbial peptide over-expression (experimental sample; n=3) and controls (UAS-AMP alone not crossed to da-GAL4; n=3) were determined using Affymetrix Drosophila Genome 2.0 Arrays.
2010-12-21 | E-GEOD-23902 | biostudies-arrayexpress
Project description:PML nuclear bodies (NBs) recruit partner proteins -including p53 and its regulators- controlling their abundance or function. Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation promotes NB-biogenesis. Yet, physiological links between PML and oxidative stress response in vivo remain unexplored. Here we identify PML as a reactive oxygen species (ROS) sensor. Pml-/- cells accumulate ROS, while PML expression decreases ROS levels. Unexpectedly, Pml-/- embryos survive acute glutathione depletion. Moreover, Pml-/- animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosis. Molecularly, Pml-/- animals fail to properly activate oxidative stress-responsive p53 targets, while NRF2 response is accelerated. Finally, in an oxidative stress-prone background, Pml-/- animals display a longevity phenotype, likely reflecting decreased basal p53 activation. Thus, similar to p53, PML exerts basal anti-oxidant properties, but also drives oxidative stress-induced changes in cell survival/proliferation or metabolism in vivo. Through NB-biogenesis, PML therefore couples ROS-sensing to p53 responses, shedding a new light on PML role in senescence or stem cell biology.
2017-09-22 | GSE103642 | GEO
Project description:It is well appreciated that reactive oxygen species (ROS) are deleterious to mammals, including humans, especially when generated in abnormally large quantities from cellular metabolism. Whereas the mechanisms leading to the production of ROS are rather well delineated, the mechanisms underlying tissue susceptibility or tolerance to oxidant stress remain elusive. Through an experimental selection over many generations, we have previously generated Drosophila melanogaster flies that tolerate tremendous oxidant stress and have shown that the family of antimicrobial peptides (AMP) is over-represented in these tolerant flies. Furthermore, we have also demonstrated that overexpression of even one AMP at a time (e.g. Diptericin) allows wild type flies to survive much better in hyperoxia. In the current study, we used a number of experimental approaches to investigate the potential mechanisms underlying hyperoxia tolerance in flies with antimicrobial peptide overexpression. We demonstrate that flies with Diptericin overexpression resist oxidative stress by increasing antioxidant enzyme activities and preventing an increase in ROS level after hyperoxia. Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirming that enhanced survival observed in these flies is related to improved redox homeostasis. We conclude that a) AMPs play an important role in tolerance to oxidant stress; b) overexpression of Diptericin changes the cellular redox balance between oxidant and antioxidant, and c) this change in redox balance plays an important role in survival in hyperoxia.
2010-12-21 | GSE23902 | GEO
Project description:Disruption of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how nearly lethal stresses affect circadian clocks. We found that near-lethal doses of reactive oxygen species (ROS)-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1. Casein kinase II (CK2) –mediated phosphorylation regulates dimerization and function of BMAL1 and HSF1 to control the cOS-evoked responses. The core cOS-responsive transcriptome includes CK2-orchestrated crosstalk between the circadian, HSR, NFκB-mediated anti-apoptotic, and Nrf2-mediated anti-oxidant pathways. This novel circadian-adaptive signaling system likely plays fundamental protective roles in ROS-inducible disorders, various diseases, and death.
2013-11-09 | GSE47955 | GEO
Project description:Male germ cells from young and aged Rats were Isolated and cultured and then treated with pro-oxidant SIN-1 and antioxidant EUK134 Study of the response of isolated male germ cells from young and aged Brown Norway Rats to oxidative stress.
2015-04-30 | GSE66976 | GEO
Project description:Bovine embryos are typically cultured at reduced oxygen tension to lower the impact of oxidative stress on embryo development. However, oocyte in vitro maturation (IVM) is performed at atmospheric oxygen tension since low oxygen during maturation has a negative impact on oocyte developmental competence. Lycopene, a carotenoid, acts as a powerful antioxidant and may protect the oocyte against oxidative stress during maturation at atmospheric oxygen conditions. Here, we assessed the effect of adding 0.2 μM lycopene (antioxidant), 5 μM menadione (pro-oxidant), and their combination on reactive oxygen species (ROS) generation in mature oocytes and subsequent blastocyst development, quality, and transcriptome in a bovine in vitro model. ROS fluorescent intensity in mature oocytes was significantly lower in the lycopene group, and resulting embryos showed a significantly higher blastocyst rate on day 8 and lower apoptotic cell ratio than all other groups. Transcriptomic analysis disclosed a total of 296 differentially expressed genes (Benjamin-Hochberg adjusted P < 0.05 and ≥ 1 log2 fold change) between lycopene and control groups with pathways associated with cellular function, metabolism, DNA repair, and anti-apoptosis upregulated in lycopene. Lycopene supplementation in serum-free maturation medium neutralizes excess ROS during maturation, enhances blastocyst development and quality, and modulates the transcriptomic landscape.
2022-01-06 | GSE192908 | GEO
Project description:Oxidative stress illustrates an imbalance between radical formation and removal. Frequent redox stress is critically involved in a variety of human pathologies including cancer, psoriasis, and chronic wounds. However, reactive species pursue a dual role being involved in signaling on the one hand and oxidative damage on the other. Using a HaCaT keratinocyte cell culture model, we here aimed at investigating the cellular and transcriptional response to periodic, low dose oxidative challenge over three months. Chronic redox stress was generated by frequent incubation with cold physical plasma treated cell culture medium. Using mRNA microarray technology, we found both acute ROS stress responses as well as numerous adaptions on the transcriptional level and over several weeks of redox challenge. This included an altered expression of 260 genes that function in inflammation and redox homeostasis, such as, signaling molecules, cytokines, and anti-oxidant enzymes. Apoptotic signaling was affected to a minor extend, especially in p53 down-stream targets. Strikingly, the anti-apoptotic heat shock protein HSP27 was strongly upregulated. These results suggest a variety of adaptive responses relating involved a number of cellular processes elicited by frequent redox stress over several months. They may help to better understand inflammatory responses in redox related diseases and possibly allow uncovering new biomarkers of ROS-stress. Microarrays were used to analyze and investigate the biological effects of repeated exposure of cold physical plasma on human HaCaT keratinocytes. Using an argon plasma jet kinpen, regulated transcripts were analyzed and further described in Schmidt et al. (submittes): âLong-term exposure to cold plasma-generated ROS âan in vitro model for redox-related diseases of the skinâ. HaCaT keratinocytes exposed to plasma treated medium - time course
2015-11-11 | E-GEOD-74876 | biostudies-arrayexpress