Hepatitis B virus X protein increases the IL-1β-induced NF-κB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT)

Chen, Wan-nan; Liu, Lingling; Jiao, Bo-Yan; Lin, Wei; Lin, Xi Zhang; Lin, Xu

doi:10.1016/j.virusres.2014.10.025

Cited by 14 publications

(14 citation statements)

References 53 publications

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“…HBx may also upregulate p-AKT protein expression levels as a mechanism to minimize oxidative damage in hepatocytes, although it was observed in this study that the antioxidant effect of p-AKT was insufficient to reverse the liver damage caused by HBx. However, HBx-induced upregulation of MAPK, NF-κB and PI3K is considered an important factor in the development of HCC (34,38,39), and abnormal activation of NF-κB in liver cancer tissue has been reported to inhibit apoptosis and promote liver cell proliferation, contributing to cancer development (38).…”

Section: Discussionmentioning

confidence: 99%

“…IL-1β promotes neutrophil migration to the liver, phagocytosis and pathogen elimination, regulates tumor growth and is associated with the invasion and metastasis of liver cancer (51,52). In addition, Chen et al (38) have demonstrated that HBx increases IL-1 secretion and induces NF-kB activation by interacting with an evolutionarily-conserved signaling intermediate in the Toll pathway. IL-18 is a pro-inflammatory cytokine that mediates the inflammatory cascade reaction and is a factor in acute liver injury (53).…”

Section: Discussionmentioning

confidence: 99%

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Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes

et al. 2020

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Hepatitis B virus x protein (HBx) serves an important role in the pathogenesis of the hepatitis B virus infection. Previous studies have reported that the interaction between HBx and hepatocyte mitochondria is an important factor leading to liver cell injury and apoptosis, ultimately inducing the formation of liver cancer. In the present study, a mouse model expressing HBx was constructed using hydrodynamic in vivo transfection based on the interaction between HBx and cytochrome c oxidase (COX) subunit III. The specific mechanism of HBx-induced oxidative stress in mouse hepatocytes and the subsequent effect on mitochondrial function and inflammatory injury was assessed. The results demonstrated that HBx reduced the activity of COX and the expression of superoxide dismutase and upregulated the expression of malondialdehyde, NF-κB and phospho-AKT, thus increasing oxidative stress. In addition, HBx induced an increase in interleukin (IL)-6, IL-1β and IL-18 expression levels, which created an inflammatory microenvironment in the liver, further promoting hepatocyte inflammatory injury. Therefore, it was proposed that HBx may affect hepatocyte mitochondrial respiration by reducing the activity of cytochrome c oxidase, leading to mitochondrial dysfunction and inducing hepatocyte inflammation and injury.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes

et al. 2020

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“…NF-κB is induced by several HBV-driven mechanisms, including generation of ROS in mitochondria [260], suppression of multiple cytoplasmic inhibitors of rel-related proteins [315] as well as of selenoprotein P, leading to enhanced lipid peroxidation [302]. In turn, NF-κB activation leads to the induction of proinflammatory cytokines, including TNFα [302, 316, 317], lymphotoxin-α [318], IL-1β [316, 319], and IL-6 [320], as well as interferon γ [321] and a chemokine interferon-gamma inducible protein 10 (IP-10) [322]. The induction of proinflammatory cytokines (IL-6, TNF-α) in HBx-expressing cells is augmented by a high fat diet/fatty acids through the efflux of calcium ions from ER stores and consequent overproduction of ROS [323].…”

Section: Hepatitis C Virusmentioning

confidence: 99%

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

et al. 2016

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Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.

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“…IL-1β was reported to stimulate NF-κB signaling pathway ( Chen et al ., 2015 ; Ji et al ., 2017 ). Also, IL-1β augmented TNF signaling through the upregulation of TNF secretion and TNFR1 cell surface expression ( Jayaraman et al ., 2013 ).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of the Expression of Matrix Metalloproteinases in Articular Chondrocytes by Resveratrol through Affecting Nuclear Factor-Kappa B Signaling Pathway

Kang

Lee

et al. 2018

Biomolecules & Therapeutics

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In the present study, we tried to examine whether resveratrol regulates the expression of matrix metalloproteinases (MMPs) through affecting nuclear factor-kappa B (NF-κB) in articular chondrocytes. Rabbit articular chondrocytes were cultured in a monolayer, and reverse transcription-polymerase chain reaction (RT-PCR) was used to measure interleukin-1β (IL-1β)-induced gene expression of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), ADAMTS-5 and type II collagen. Effect of resveratrol on IL-1β-induced secretion of MMP-3 was investigated in rabbit articular chondrocytes using western blot analysis. To elucidate the action mechanism of resveratrol, effect of resveratrol on IL-1β-induced NF-κB signaling pathway was investigated in SW1353, a human chondrosarcoma cell line, by western blot analysis. The results were as follows: (1) resveratrol inhibited the gene expression of MMP-3, MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5, but increased the gene expression of type II collagen; (2) resveratrol reduced the secretion of MMP-3; (3) resveratrol inhibited IL-1β-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Bα (IκBα); (4) resveratrol inhibited IL-1β-induced phosphorylation and nuclear translocation of NF-κB p65. This, in turn, led to the down-regulation of gene expression of MMPs in SW1353 cells. These results suggest that resveratrol can regulate the expression of MMPs through affecting NF-κB by directly acting on articular chondrocytes.

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Hepatitis B virus X protein increases the IL-1β-induced NF-κB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT)

Cited by 14 publications

References 53 publications

Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes

Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

Inhibition of the Expression of Matrix Metalloproteinases in Articular Chondrocytes by Resveratrol through Affecting Nuclear Factor-Kappa B Signaling Pathway

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