scholarly journals Increasing Oxygen Partial Pressures Induce a Distinct Transcriptional Response in Human PBMC: A Pilot Study on the “Normobaric Oxygen Paradox”

2021 ◽  
Vol 22 (1) ◽  
pp. 458
Author(s):  
Deborah Fratantonio ◽  
Fabio Virgili ◽  
Alessandro Zucchi ◽  
Kate Lambrechts ◽  
Tiziana Latronico ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Oxidative Stress Response ◽  
Molecular Characteristics ◽  
Nuclear Factor ◽  
Normobaric Oxygen ◽  
Oxygen Paradox

The term “normobaric oxygen paradox” (NOP), describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as oxygen shortage, and resulting in up-regulation of the Hypoxia-inducible factor 1α (HIF-1α) transcription factor activity. The molecular characteristics of this response have not been yet fully characterized. Herein, we report the activation time trend of oxygen-sensitive transcription factors in human peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects after one hour of exposure to mild (MH), high (HH) and very high (VHH) hyperoxia, corresponding to 30%, 100%, 140% O2, respectively. Our observations confirm that MH is perceived as a hypoxic stress, characterized by the activation of HIF-1α and Nuclear factor (erythroid-derived 2)-like 2 (NRF2), but not Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Conversely, HH is associated to a progressive loss of NOP response and to an increase in oxidative stress leading to NRF2 and NF-kB activation, accompanied by the synthesis of glutathione (GSH). After VHH, HIF-1α activation is totally absent and oxidative stress response, accompanied by NF-κB activation, is prevalent. Intracellular GSH and Matrix metallopeptidase 9 (MMP-9) plasma levels parallel the transcription factors activation pattern and remain elevated throughout the observation time. In conclusion, our study confirms that, in vivo, the return to normoxia after MH is sensed as a hypoxic trigger characterized by HIF-1α activation. On the contrary, HH and VHH induce a shift toward an oxidative stress response, characterized by NRF2 and NF-κB activation in the first 24 h post exposure.

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.

scholarly journals The transcription factor, Nuclear factor, erythroid 2 (Nfe2), is a regulator of the oxidative stress response during Danio rerio development

2016 ◽  
Vol 180 ◽  
pp. 141-154 ◽  
Author(s):  
Larissa M. Williams ◽  
Briony A. Lago ◽  
Andrew G. McArthur ◽  
Amogelang R. Raphenya ◽  
Nicholas Pray ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Stress Response ◽  
Danio Rerio ◽  
Oxidative Stress Response ◽  
Nuclear Factor ◽  
Transcription Factor Nuclear Factor

scholarly journals Kynurenine Metabolism Lifespan Extension Mediated by Oxidative Stress Response and Hypoxic Response in C. elegans

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 684-684
Author(s):  
Raul Castro-Portuguez ◽  
Jeremy Meyers ◽  
Sam Freitas ◽  
Hope Dang ◽  
Emily Turner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Aging Process ◽  
De Novo ◽  
Kynurenine Pathway ◽  
Oxidative Stress Response ◽  
Lifespan Extension ◽  
Hypoxic Stress ◽  
C Elegans

Abstract Aging is characterized by a progressive decline in the normal physiological functions of an organism, ultimately leading to mortality. Metabolic changes throughout the aging process disrupt the balance and homeostasis of the cell. The kynurenine metabolic pathway is the sole de novo biosynthetic pathway for producing NAD+ from ingested tryptophan. Altered kynurenine pathway activity is associated with both aging and a variety of age-associated diseases, and kynurenine-based interventions can extend lifespan in Caenorhabditis elegans. Our laboratory recently demonstrated knockdown of the kynurenine pathway enzymes kynureninase (KYNU) or 3-hydroxyanthranilic acid dioxygenase (HAAO) increases lifespan by 20-30% in C elegans. However, the mechanism of how these interventions may modulate response against different stressors during the aging process has yet to be explored. Fluorescent reporter strains show the stress-responsive transcription factors skn-1 (ortholog of NRF2/NFE2L2; oxidative stress response) and hif-1 (ortholog of HIF1A; hypoxic stress response) to be highly upregulated when the kynurenine pathway is inhibited. We also demonstrated the increase expression of gst-4 and gcs-1 (transcriptional targets skn-1), which are involved in production of the antioxidant glutathione (GSH), as well as upregulation of cysl-2 (transcriptional target of hif-1), a regulator of cysteine biosynthesis from serine. We hypothesize that lifespan extension resulting from kynurenine pathway inhibition is mediated, at least in part, by upregulation of these transcription factors, providing elevated defense against oxidative stress and hypoxic stress.

scholarly journals Nuclear Matrix Protein (NRP/B) Modulates the Nuclear Factor (Erythroid-derived 2)-related 2 (NRF2)-dependent Oxidative Stress Response

2010 ◽  
Vol 285 (34) ◽  
pp. 26190-26198 ◽  
Author(s):  
Seyha Seng ◽  
Hava Karsenty Avraham ◽  
Gabriel Birrane ◽  
Shuxian Jiang ◽  
Shalom Avraham
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Nuclear Matrix ◽  
Matrix Protein ◽  
Oxidative Stress Response ◽  
Nuclear Factor ◽  
Nuclear Matrix Protein

scholarly journals Xrp1 and Irbp18 trigger a feed-forward loop of proteotoxic stress to induce the loser status

PLoS Genetics ◽  
2021 ◽  
Vol 17 (12) ◽  
pp. e1009946
Author(s):  
Paul F. Langton ◽  
Michael E. Baumgartner ◽  
Remi Logeay ◽  
Eugenia Piddini
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Wild Type ◽  
Cell Competition ◽  
Feed Forward ◽  
Feed Forward Loop ◽  
Proteotoxic Stress

Cell competition induces the elimination of less-fit “loser” cells by fitter “winner” cells. In Drosophila, cells heterozygous mutant in ribosome genes, Rp/+, known as Minutes, are outcompeted by wild-type cells. Rp/+ cells display proteotoxic stress and the oxidative stress response, which drive the loser status. Minute cell competition also requires the transcription factors Irbp18 and Xrp1, but how these contribute to the loser status is partially understood. Here we provide evidence that initial proteotoxic stress in RpS3/+ cells is Xrp1-independent. However, Xrp1 is sufficient to induce proteotoxic stress in otherwise wild-type cells and is necessary for the high levels of proteotoxic stress found in RpS3/+ cells. Surprisingly, Xrp1 is also induced downstream of proteotoxic stress, and is required for the competitive elimination of cells suffering from proteotoxic stress or overexpressing Nrf2. Our data suggests that a feed-forward loop between Xrp1, proteotoxic stress, and Nrf2 drives Minute cells to become losers.

Transcriptional control of the oxidative stress response and implications of using plant derived molecules for therapeutic interventions in cancer

2021 ◽  
Vol 28 ◽  
Author(s):  
Asim Rizvi ◽  
Mohd. Farhan ◽  
Faisal Nabi ◽  
Rizwan Hasan Khan ◽  
Mohd. Adil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Cancer Cells ◽  
Transcriptional Control ◽  
Regulation Of Gene Expression ◽  
Oxidative Stress Response ◽  
Therapeutic Interventions ◽  
Lead Compounds

: Oxidative stress response is critical for the malignant cells. It plays dual role by helping cancer cells survive and proliferate but also causing apoptosis and apoptosis like cell death. The oxidative stress response is characterized by a tight regulation of gene expression by a series of transcription factors (OSRts; oxidative stress response transcription factors). In this communication, we review the role of OSRts, notably NRF2 and p53 as well as other transcription factors, that modulate the response. We discuss how the oxidative stress response is hierarchal and controls ‘live or die’ signals. This is followed by a discussion on how plant derived molecules, including polyphenols, which are described both as prooxidants and antioxidants within the cancer cells, have been reported to affect the activities of OSRts. Deriving an example from preliminary data from our group, we discuss how plant derived molecules might modulate the oxidative stress response by causing structural perturbations in the proteinacious transcription factors, notably Nrf2 and p53. We look at this information in the light of understanding how plant derived molecules maybe used as lead compounds to develop modulators of the oxidative stress response.

scholarly journals The Role of Nuclear Factor-E2-Related Factor 1 in the Oxidative Stress Response in MC3T3-E1 Osteoblastic Cells

2016 ◽  
Vol 31 (2) ◽  
pp. 336 ◽  
Author(s):  
So Young Park ◽  
Sung Hoon Kim ◽  
Hyun Koo Yoon ◽  
Chang Hoon Yim ◽  
Sung-Kil Lim
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Osteoblastic Cells ◽  
Related Factor ◽  
Nuclear Factor

scholarly journals Association of the Skn7 and Yap1 Transcription Factors in the Saccharomyces cerevisiae Oxidative Stress Response

2011 ◽  
Vol 10 (6) ◽  
pp. 761-769 ◽  
Author(s):  
K. E. Mulford ◽  
J. S. Fassler
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Transcription Factors ◽  
Stress Response ◽  
Wall Stress ◽  
Oxidative Stress Response ◽  
Independent Manner ◽  
Content Type ◽  
Stress Response Genes ◽  
Two Factors

ABSTRACT Saccharomyces cerevisiae Skn7p is a stress response transcription factor that undergoes aspartyl phosphorylation by the Sln1p histidine kinase. Aspartyl phosphorylation of Skn7p is required for activation of genes required in response to wall stress, but Skn7p also activates oxidative stress response genes in an aspartyl phosphorylation-independent manner. The presence of binding sites for the Yap1p and Skn7p transcription factors in oxidative stress response promoters and the oxidative stress-sensitive phenotypes of SKN7 and YAP1 mutants suggest that these two factors work together. We present here evidence for a DNA-independent interaction between the Skn7 and Yap1 proteins that involves the receiver domain of Skn7p and the cysteine-rich domains of Yap1p. The interaction with Yap1p may help partition the Skn7 protein to oxidative stress response promoters when the Yap1 protein accumulates in the nucleus.

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