Orphan Nuclear Receptor Pregnane X Receptor Sensitizes Oxidative Stress Responses in Transgenic Mice and Cancerous Cells

Lithium cobalt oxide (LiCoO2), an example of nanoscale transition metal oxide and a widely commercialized cathode material in lithium ion batteries, has been shown to induce oxidative stress and generate intracellular reactive oxygen species (ROS) in model organisms.

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The Arabidopsis mediator complex subunit 8 regulates oxidative stress responses

The Plant Cell ◽

10.1093/plcell/koab079 ◽

2021 ◽

Cited By ~ 1

Author(s):

Huaming He ◽

Jordi Denecker ◽

Katrien Van Der Kelen ◽

Patrick Willems ◽

Robin Pottie ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Salicylic Acid ◽

Jasmonic Acid ◽

Stress Responses ◽

Negative Regulator ◽

Mediator Complex ◽

Defense Gene Expression ◽

A Genome ◽

Oxidative Stress Responses

Abstract Signaling events triggered by hydrogen peroxide (H2O2) regulate plant growth and defense by orchestrating a genome-wide transcriptional reprogramming. However, the specific mechanisms that govern H2O2-dependent gene expression are still poorly understood. Here, we identify the Arabidopsis Mediator complex subunit MED8 as a regulator of H2O2 responses. The introduction of the med8 mutation in a constitutive oxidative stress genetic background (catalase-deficient, cat2) was associated with enhanced activation of the salicylic acid pathway and accelerated cell death. Interestingly, med8 seedlings were more tolerant to oxidative stress generated by the herbicide methyl viologen (MV) and exhibited transcriptional hyperactivation of defense signaling, in particular salicylic acid- and jasmonic acid-related pathways. The med8-triggered tolerance to MV was manipulated by the introduction of secondary mutations in salicylic acid and jasmonic acid pathways. In addition, analysis of the Mediator interactome revealed interactions with components involved in mRNA processing and microRNA biogenesis, hence expanding the role of Mediator beyond transcription. Notably, MED8 interacted with the transcriptional regulator NEGATIVE ON TATA-LESS, NOT2, to control the expression of H2O2-inducible genes and stress responses. Our work establishes MED8 as a component regulating oxidative stress responses and demonstrates that it acts as a negative regulator of H2O2-driven activation of defense gene expression.

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Clade III cytokinin response factors share common roles in response to oxidative stress responses linked to cytokinin synthesis

Journal of Experimental Botany ◽

10.1093/jxb/erab076 ◽

2021 ◽

Vol 72 (8) ◽

pp. 3294-3306

Author(s):

Ariel M Hughes ◽

H Tucker Hallmark ◽

Lenka Plačková ◽

Ondrej Novák ◽

Aaron M Rashotte

Keyword(s):

Oxidative Stress ◽

Transcription Factors ◽

Stress Response ◽

Stress Responses ◽

Oxidative Stress Response ◽

Response Factors ◽

Ontology Term ◽

Regulated Expression ◽

Cytokinin Response ◽

Oxidative Stress Responses

Abstract Cytokinin response factors (CRFs) are transcription factors that are involved in cytokinin (CK) response, as well as being linked to abiotic stress tolerance. In particular, oxidative stress responses are activated by Clade III CRF members, such as AtCRF6. Here we explored the relationships between Clade III CRFs and oxidative stress. Transcriptomic responses to oxidative stress were determined in two Clade III transcription factors, Arabidopsis AtCRF5 and tomato SlCRF5. AtCRF5 was required for regulated expression of >240 genes that are involved in oxidative stress response. Similarly, SlCRF5 was involved in the regulated expression of nearly 420 oxidative stress response genes. Similarities in gene regulation by these Clade III members in response to oxidative stress were observed between Arabidopsis and tomato, as indicated by Gene Ontology term enrichment. CK levels were also changed in response to oxidative stress in both species. These changes were regulated by Clade III CRFs. Taken together, these findings suggest that Clade III CRFs play a role in oxidative stress response as well as having roles in CK signaling.

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Biotransformation and oxidative stress responses in rat hepatic cell-line (H4IIE) exposed to organophosphate esters (OPEs)

Toxicology and Applied Pharmacology ◽

10.1016/j.taap.2019.04.004 ◽

2019 ◽

Vol 371 ◽

pp. 84-94 ◽

Cited By ~ 11

Author(s):

Elvira Mennillo ◽

Francesca Cappelli ◽

Augustine Arukwe

Keyword(s):

Oxidative Stress ◽

Cell Line ◽

Stress Responses ◽

Hepatic Cell ◽

Organophosphate Esters ◽

Hepatic Cell Line ◽

Oxidative Stress Responses ◽

And Oxidative Stress

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Endothelial PPAR-γ provides vascular protection from IL-1β-induced oxidative stress

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00490.2015 ◽

2016 ◽

Vol 310 (1) ◽

pp. H39-H48 ◽

Cited By ~ 20

Author(s):

Masashi Mukohda ◽

Madeliene Stump ◽

Pimonrat Ketsawatsomkron ◽

Chunyan Hu ◽

Frederick W. Quelle ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Endothelial Dysfunction ◽

Nitric Oxide Synthase ◽

Transgenic Mice ◽

Stress Responses ◽

Endothelial Nitric Oxide Synthase ◽

Ppar Γ ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Loss of peroxisome proliferator-activated receptor (PPAR)-γ function in the vascular endothelium enhances atherosclerosis and NF-κB target gene expression in high-fat diet-fed apolipoprotein E-deficient mice. The mechanisms by which endothelial PPAR-γ regulates inflammatory responses and protects against atherosclerosis remain unclear. To assess functional interactions between PPAR-γ and inflammation, we used a model of IL-1β-induced aortic dysfunction in transgenic mice with endothelium-specific overexpression of either wild-type (E-WT) or dominant negative PPAR-γ (E-V290M). IL-1β dose dependently decreased IκB-α, increased phospho-p65, and increased luciferase activity in the aorta of NF-κB-LUC transgenic mice. IL-1β also dose dependently reduced endothelial-dependent relaxation by ACh. The loss of ACh responsiveness was partially improved by pretreatment of the vessels with the PPAR-γ agonist rosiglitazone or in E-WT. Conversely, IL-1β-induced endothelial dysfunction was worsened in the aorta from E-V290M mice. Although IL-1β increased the expression of NF-κB target genes, NF-κB p65 inhibitor did not alleviate endothelial dysfunction induced by IL-1β. Tempol, a SOD mimetic, partially restored ACh responsiveness in the IL-1β-treated aorta. Notably, tempol only modestly improved protection in the E-WT aorta but had an increased protective effect in the E-V290M aorta compared with the aorta from nontransgenic mice, suggesting that PPAR-γ-mediated protection involves antioxidant effects. IL-1β increased ROS and decreased the phospho-endothelial nitric oxide synthase (Ser1177)-to-endothelial nitric oxide synthase ratio in the nontransgenic aorta. These effects were completely abolished in the aorta with endothelial overexpression of WT PPAR-γ but were worsened in the aorta with E-V290M even in the absence of IL-1β. We conclude that PPAR-γ protects against IL-1β-mediated endothelial dysfunction through a reduction of oxidative stress responses but not by blunting IL-1β-mediated NF-κB activity.

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