Porcine Circovirus 2 Activates the PERK-Reactive Oxygen Species Axis To Induce p53 Phosphorylation with Subsequent Cell Cycle Arrest at S Phase in Favor of Its Replication

Deng, Zhuofan; Sun, Renjie; Han, Xiao; Zhang, Yikai; Zhou, Yingshan; Shan, Ying; Xu, Jie; Li, Xiaoliang; He, Fang; Fang, Weihuan

doi:10.1128/jvi.01274-22

Cited by 4 publications

(4 citation statements)

References 64 publications

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“…It is likely that the intracellularly accumulated Aβ in the patient with APP‐E693Δ induces ATG4A expression at the transcriptional level. Although the responsible transcription factors are unknown, the p53 family and nuclear transcription factor‐Y are candidates because they are activated by oxidative or ER stresses (Deng et al, 2022; Yoshida et al, 2001) that can be induced by intracellular Aβ (Kondo et al, 2013), and their consensus upstream DNA sequences are in the 5′ untranslated region of ATG4A (Huang et al, 2010). On the other hand, the mechanism of ATG4A upregulation in sporadic AD patient AD3 is currently unknown.…”

Section: Discussionmentioning

confidence: 99%

Alterations of ATG4A and LC3B in neurons derived from Alzheimer's disease patients

et al. 2023

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We investigated the alterations in autophagy-related molecules in neurons differentiated from induced pluripotent stem cells obtained from patients with Alzheimer's disease (AD). Consistent with our previous microarray data, ATG4A protein was upregulated in the neurons derived from a familial AD patient with an APP-E693Δ mutation who showed accumulation of intracellular amyloid β peptide (Aβ). This upregulation was reversed by inhibiting Aβ production, suggesting that the intracellular Aβ may be responsible for the upregulation of ATG4A. The LC3B-II/LC3B-I ratio, an index of autophagosome formation, was lower in the neurons derived from the AD patient with APP-E693Δ as well as the neurons derived from other familial and sporadic AD patients. These findings indicate that dysregulation of autophagy-related molecules may accelerate the pathogenesis of AD.

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Section: Discussionmentioning

confidence: 99%

Alterations of ATG4A and LC3B in neurons derived from Alzheimer's disease patients

et al. 2023

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“…ROS mediates cell damage, activates 5’ adenosine monophosphate-activated protein kinase and pancreatic endoplasmic reticulum kinase-like endoplasmic reticulum kinase, and increases the levels of hypoxia-inducible factor (HIF)-1 and nuclear factor κB (NF-κB) [ 15 ]. Activate 5’ adenosine monophosphate-activated protein kinase plays a role in glucose uptake and glycolysis and activates HIF-1; HIF-1 plays a role in transcription, translation, and stability [ 16 ]; NF-κB induces cytokines, chemokines, and HIF-1 [ 17 ]; and protein kinase RNA-like ER kinase induces unfolded protein response and inhibits protein synthesis [ 18 ]. An increase in free cytosolic Ca 2+ is a general mediator of cell death.…”

Section: Hypoxia and Ibdmentioning

confidence: 99%

Hypoxia, hypoxia-inducible factors and inflammatory bowel diseases

Hou,

Bian,

Jing

et al. 2023

Gastroenterology Report

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Adequate oxygen supply is essential for maintaining the body's normal physiological function. In chronic inflammatory conditions such as inflammatory bowel disease (IBD), insufficient oxygen reaching the intestine triggers the regulatory system in response to environmental changes. However, the pathogenesis of IBD is still under investigation. Recent research has highlighted the significant role of hypoxia in IBD, particularly the involvement of hypoxia-inducible factors (HIF) and their regulatory mechanisms, making them promising therapeutic targets for IBD. This review will delve into the role of hypoxia, HIF, and the associated hypoxia-inflammatory microenvironment in the context of IBD. Potential interventions for addressing these challenging gastrointestinal inflammatory diseases will also be discussed within this framework.

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“… 2018 ; Deng et al. 2022 ). The PERK-ROS axis promotes p53 upregulation in PCV2 inoculated PAMs and the accumulated phosphorylated p53 leads to cell cycle arrest at S-phase and enhances viral replication.…”

Section: Immunomodulatory Elements Of Circovirusesmentioning

confidence: 99%

“…It remains a question whether this phenomenon is associated with ORF5 (Deng et al. 2022 ). In other experimental design, the prolongation of the S-phase has been retrieved in PAMs by ORF5 (Lv et al.…”

Section: Immunomodulatory Elements Of Circovirusesmentioning

confidence: 99%

Mechanisms of circovirus immunosuppression and pathogenesis with a focus on porcine circovirus 2: a review

Fehér

Jakab

Bányai

2023

Veterinary Quarterly

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Certain pathogens, due to their adverse effects on the immune reaction, aggravate the course of concomitant heterologous infections. Here we summarize mechanisms by which circoviruses, including the most studied porcine circovirus 2, and other mammalian and avian circoviruses, trigger their own replication and confound the hosts’ immune response. At different stages of infection, from latent state to disease induction, these viruses markedly influence the cellular signaling pathways. Circoviruses have been found to interfere with interferon and proinflammatory cytokine producing and responsive pathways. Apoptotic processes, altered cellular transport and constraint of the mitotic phase all support the viral replication. The cytokine imbalance and lymphocyte depletion, thus the impaired immunity, favors invasion of super- or co-infecting agents, which in concert with circoviruses induce illnesses with increased severity. The information summarized in this review point out the diversity of host and viral factors involved in the mechanisms of disease progression during circovirus infections.

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Porcine Circovirus 2 Activates the PERK-Reactive Oxygen Species Axis To Induce p53 Phosphorylation with Subsequent Cell Cycle Arrest at S Phase in Favor of Its Replication

Abstract: Coinfections or noninfectious triggers have long been considered to potentiate PCV2 infection, leading to manifestation of PCVAD. The triggering mechanisms remain largely unknown.

Cited by 4 publications

References 64 publications

Alterations of ATG4A and LC3B in neurons derived from Alzheimer's disease patients

Alterations of ATG4A and LC3B in neurons derived from Alzheimer's disease patients

Hypoxia, hypoxia-inducible factors and inflammatory bowel diseases

Mechanisms of circovirus immunosuppression and pathogenesis with a focus on porcine circovirus 2: a review

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