scholarly journals Cellular oxidative stress response mediates radiosensitivity in Fus1-deficient mice

2015 ◽  
Vol 6 (2) ◽  
pp. e1652-e1652 ◽  
Author(s):  
E M Yazlovitskaya ◽  
P A Voziyan ◽  
T Manavalan ◽  
W G Yarbrough ◽  
A V Ivanova
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Deficient Mice

scholarly journals Bach1Deficiency and Accompanying Overexpression of Heme Oxygenase-1 Do Not Influence Aging or Tumorigenesis in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Kazushige Ota ◽  
Andrey Brydun ◽  
Ari Itoh-Nakadai ◽  
Jiying Sun ◽  
Kazuhiko Igarashi
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Heme Oxygenase ◽  
Transcriptional Activity ◽  
Oxidative Stress Response ◽  
Acute Injury ◽  
Heme Oxygenase 1 ◽  
Wild Type ◽  
Environmental Perturbations ◽  
Deficient Mice

Oxidative stress contributes to both aging and tumorigenesis. The transcription factor Bach1, a regulator of oxidative stress response, augments oxidative stress by repressing the expression of heme oxygenase-1 (HO-1) gene (Hmox1) and suppresses oxidative stress-induced cellular senescence by restricting the p53 transcriptional activity. Here we investigated the lifelong effects ofBach1deficiency on mice.Bach1-deficient mice showed longevity similar to wild-type mice. Although HO-1 was upregulated in the cells ofBach1-deficient animals, the levels of ROS inBach1-deficient HSCs were comparable to those in wild-type cells.Bach1−/−;p53−/−mice succumbed to spontaneous cancers as frequently asp53-deficient mice.Bach1deficiency significantly altered transcriptome in the liver of the young mice, which surprisingly became similar to that of wild-type mice during the course of aging. The transcriptome adaptation toBach1deficiency may reflect how oxidative stress response is tuned upon genetic and environmental perturbations. We concluded thatBach1deficiency and accompanying overexpression of HO-1 did not influence aging or p53 deficiency-driven tumorigenesis. Our results suggest that it is useful to target Bach1 for acute injury responses without inducing any apparent deteriorative effect.

scholarly journals Upregulation of Anti-Oxidative Stress Response Improves Metabolic Changes in L-Selectin-Deficient Mice but Does Not Prevent NAFLD Progression or Fecal Microbiota Shifts

2021 ◽  
Vol 22 (14) ◽  
pp. 7314
Author(s):  
Sreepradha Eswaran ◽  
Anshu Babbar ◽  
Hannah K. Drescher ◽  
Thomas C. A. Hitch ◽  
Thomas Clavel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Stress Response ◽  
Immune Cell ◽  
Fecal Microbiota ◽  
Oxidative Stress Response ◽  
Metabolic Changes ◽  
Related Factor ◽  
Alcoholic Fatty Liver ◽  
Deficient Mice

(1) Background: Non-alcoholic fatty liver disease (NAFLD) is a growing global health problem. NAFLD progression involves a complex interplay of imbalanced inflammatory cell populations and inflammatory signals such as reactive oxygen species and cytokines. These signals can derive from the liver itself but also from adipose tissue or be mediated via changes in the gut microbiome. We analyzed the effects of a simultaneous migration blockade caused by L-selectin-deficiency and an enhancement of the anti-oxidative stress response triggered by hepatocytic Kelch-like ECH-associated protein 1 (Keap1) deletion on NAFLD progression. (2) Methods: L-selectin-deficient mice (Lsel−/−Keap1flx/flx) and littermates with selective hepatic Keap1 deletion (Lsel−/−Keap1Δhepa) were compared in a 24-week Western-style diet (WD) model. (3) Results: Lsel−/−Keap1Δhepa mice exhibited increased expression of erythroid 2-related factor 2 (Nrf2) target genes in the liver, decreased body weight, reduced epidydimal white adipose tissue with decreased immune cell frequencies, and improved glucose response when compared to their Lsel−/−Keap1flx/flx littermates. Although WD feeding caused drastic changes in fecal microbiota profiles with decreased microbial diversity, no genotype-dependent shifts were observed. (4) Conclusions: Upregulation of the anti-oxidative stress response improves metabolic changes in L-selectin-deficient mice but does not prevent NAFLD progression and shifts in the gut microbiota.

scholarly journals Environmental Conditions Modulate the Transcriptomic Response of Both Caulobacter crescentus Morphotypes to Cu Stress

2021 ◽  
Vol 9 (6) ◽  
pp. 1116
Author(s):  
Laurens Maertens ◽  
Pauline Cherry ◽  
Françoise Tilquin ◽  
Rob Van Houdt ◽  
Jean-Yves Matroule
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Stress Responses ◽  
Caulobacter Crescentus ◽  
Oxidative Stress Response ◽  
Transport Systems ◽  
Transcriptomic Response ◽  
Swarmer Cell ◽  
Cu Stress ◽  
Cellular Environment

Bacteria encounter elevated copper (Cu) concentrations in multiple environments, varying from mining wastes to antimicrobial applications of copper. As the role of the environment in the bacterial response to Cu ion exposure remains elusive, we used a tagRNA-seq approach to elucidate the disparate responses of two morphotypes of Caulobacter crescentus NA1000 to moderate Cu stress in a complex rich (PYE) medium and a defined poor (M2G) medium. The transcriptome was more responsive in M2G, where we observed an extensive oxidative stress response and reconfiguration of the proteome, as well as the induction of metal resistance clusters. In PYE, little evidence was found for an oxidative stress response, but several transport systems were differentially expressed, and an increased need for histidine was apparent. These results show that the Cu stress response is strongly dependent on the cellular environment. In addition, induction of the extracytoplasmic function sigma factor SigF and its regulon was shared by the Cu stress responses in both media, and its central role was confirmed by the phenotypic screening of a sigF::Tn5 mutant. In both media, stalked cells were more responsive to Cu stress than swarmer cells, and a stronger basal expression of several cell protection systems was noted, indicating that the swarmer cell is inherently more Cu resistant. Our approach also allowed for detecting several new transcription start sites, putatively indicating small regulatory RNAs, and additional levels of Cu-responsive regulation.

scholarly journals Meta-Analysis of Oxidative Transcriptomes in Insects

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 345
Author(s):  
Hidemasa Bono
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Meta Analysis ◽  
Adherens Junction ◽  
Enrichment Analysis ◽  
Oxidative Stress Response ◽  
Insect Species ◽  
Rna Seq ◽  
Manual Curation ◽  
Analysis Workflow

Data accumulation in public databases has resulted in extensive use of meta-analysis, a statistical analysis that combines the results of multiple studies. Oxidative stress occurs when there is an imbalance between free radical activity and antioxidant activity, which can be studied in insects by transcriptome analysis. This study aimed to apply a meta-analysis approach to evaluate insect oxidative transcriptomes using publicly available data. We collected oxidative stress response-related RNA sequencing (RNA-seq) data for a wide variety of insect species, mainly from public gene expression databases, by manual curation. Only RNA-seq data of Drosophila melanogaster were found and were systematically analyzed using a newly developed RNA-seq analysis workflow for species without a reference genome sequence. The results were evaluated by two metric methods to construct a reference dataset for oxidative stress response studies. Many genes were found to be downregulated under oxidative stress and related to organ system process (GO:0003008) and adherens junction organization (GO:0034332) by gene enrichment analysis. A cross-species analysis was also performed. RNA-seq data of Caenorhabditis elegans were curated, since no RNA-seq data of insect species are currently available in public databases. This method, including the workflow developed, represents a powerful tool for deciphering conserved networks in oxidative stress response.

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

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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