Upregulation of Akt/NF-&amp;kappa;B-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Tang, Bo; Tang, Fang; Wang, Zhenran; Qi, Guangying; Liang, Xingsi; Li, Bo; Yuan, Shengguang; Liu, Jie; Yu, Shuiping; He, Songqing

doi:10.2147/ijn.s101285

Cited by 87 publications

(54 citation statements)

References 45 publications

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“…1e, f ). Since excessive and robust pro-inflammatory cytokine production increases the severity of EV71 infection [10] and is highly relevant for apoptosis [20], production of these cytokines was investigated. The qPCR and ELISA data confirmed the significant increases in the levels of IL-1β, IL-6, and TNF-α mRNA and protein after EV71 infection (Fig.…”

Section: Ev71 Infection Stimulates Ros Production Cell Death and Inmentioning

confidence: 99%

“…These data demonstrated that Nrf2 is responsible for Keap1-mediated, EV71-induced cellular dysfunction. Because Akt phosphorylation is positively correlated with apoptosis and inflammation [18][19][20], we next assessed the effect of Nrf2 silencing on the activation of the Akt inflammatory sensor and the activity of proteins associated with cell death, including Caspase-3, Fas-L, Bax, and Fas. EV71 infection remarkably reinforced the expression of all these proteins (Fig.…”

Section: Nrf2 Expression Is Responsible For Keap1-regulated Ev71-indmentioning

confidence: 99%

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RETRACTED ARTICLE: EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells

Bai

Zhao

et al. 2020

Gut Pathog

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Background: Emerging evidence closely links Enterovirus 71 (EV71) infection with the generation of reactive oxygen species (ROS). Excess ROS results in apoptosis and exacerbates inflammatory reactions. The Keap1-Nrf2 axis serves as an essential oxidant counteracting pathway. Methods: The present study aimed to elucidate the role of the Keap1-Nrf2 pathway in modulating apoptosis and inflammatory reactions triggered by oxidative stress in Vero and RD cells upon EV71 infection. Results: Elevated ROS production was identified in EV71 infected Vero and RD cells. The percentage of dead cells and expression of inflammation-promoting cytokines were increased in these cells. EV71 infected cells also displayed reinforced Keap1 expression and abrogated Nrf2 expression. Keap1 silencing resulted in the downstream aggregation of the Nrf2 protein and heme oxygenase-1 HO-1. Keap1 silencing repressed ubiquitination and reinforced Nrf2 nuclear trafficking. Furthermore, silencing Keap1 expression repressed ROS production, cell death, and inflammatory reactions in EV71 infected RD and Vero cells. In contrast, silencing of both Keap1 and Nrf2 restored ROS production, cell death, and inflammatory reactions. Nrf2 and Keap1 modulated the stimulation of the Akt sensor and extrinsic as well as intrinsic cell death pathways, resulting in EV71-triggered cell death and inflammatory reactions. Conclusions: EV71 infection can trigger ROS production, cell death, and inflammatory reactions by modulating the Nrf2 and Keap1 levels of infected cells.

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Section: Ev71 Infection Stimulates Ros Production Cell Death and Inmentioning

confidence: 99%

Section: Nrf2 Expression Is Responsible For Keap1-regulated Ev71-indmentioning

confidence: 99%

RETRACTED ARTICLE: EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells

Bai

Zhao

et al. 2020

Gut Pathog

View full text Add to dashboard Cite

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“…Combined these responses could lead to serious health concerns if chronic exposure occurred, as alterations to these functional processes have been correlated to numerous diseases, including cancer, heart disease, and neurological disorders [ 30 , 32 , 35 ]. Moreover, increased Akt phosphorylation can trigger a deeper inflammatory response [ 36 ], thereby establishing a synergistic intracellular reaction.…”

Section: Resultsmentioning

confidence: 99%

Toxicological Implications of Platinum Nanoparticle Exposure: Stimulation of Intracellular Stress, Inflammatory Response, and Akt Signaling In Vitro

Labrador-Rached

Browning

Braydich‐Stolle

et al. 2018

Journal of Toxicology

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Due to their distinctive physicochemical properties, platinum nanoparticles (PtNPs) have emerged as a material of interest for a number of biomedical therapeutics. However, in some instances NP exposure has been correlated to health and safety concerns, including cytotoxicity, activation of cellular stress, and modification to normal cell functionality. As PtNPs have induced differential cellular responses in vitro, the goal of this study was to further characterize the behavior and toxicological potential of PtNPs within a HepG2 liver model. This study identified that a high PtNP dosage induced HepG2 cytotoxicity. However, lower, subtoxic PtNP concentrations were able to elicit multiple stress responses, secretion of proinflammatory cytokines, and modulation of insulin-like growth factor-1 dependent signal transduction. Taken together, this work suggests that PtNPs would not be overtly toxic for acute exposures, but sustained cellular interactions might produce long term health consequences.

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“…4F and G). The Akt pathway is a well-known signal transduction pathway involved in the progression of inflammation response and the Akt phosphorylation level indicates the activation of Akt (Tang et al, 2016). These results suggested that TNF/LT may regulate adipose insulin sensitivity through inflammation-independent mechanisms.…”

Section: Resultsmentioning

confidence: 99%

Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PM2.5

Chen

Zhou

et al. 2017

Toxicology

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Background Exposure to ambient fine particulate matter (PM2.5) is associated with increased cardiometabolic morbidity and mortality. This is widely believed to be attributable to PM2.5 exposure-induced pulmonary and subsequent systemic inflammation. Tumor necrosis factor alpha (TNFα), lymphotoxin α (LTα), and lymphotoxin β (LTβ) are three homologous pro-inflammatory cytokines, each with both unique and redundant activities in inflammation. Their role in PM2.5 exposure-induced inflammation and adverse cardiometabolic effects has to be determined. Methods and results LTα/TNFα/LTβ triple-knockout (TNF/LT KO) and wildtype (WT) mice were exposed to concentrated ambient PM2.5 (CAP) for 5 months. Lung pathological analysis revealed that TNF/LT deficiency reduced CAP exposure-induced pulmonary inflammation. However, glucose homeostasis assessments showed that TNF/LT deficiency significantly aggravated CAP exposure-induced glucose intolerance and insulin resistance. Consistent with glucose homeostasis assessments, CAP exposure significantly increased the body weight and adiposity of TNF/LT KO but not WT mice. In contrast to its body weight effects, CAP exposure reduced food intake of WT but not TNF/LT KO mice. On the other hand, CAP exposure induced marked fat droplet accumulation in brown adipose tissues of WT mice and significantly decreased their uncoupling protein 1 (UCP1) expression, and these effects were markedly exacerbated in TNF/LT KO mice. Conclusion The present study suggests that TNF/LT deficiency influences PM2.5 exposure-induced response of energy metabolism through alterations in both food intake and energy expenditure.

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Upregulation of Akt/NF-κB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle

Cited by 87 publications

References 45 publications

RETRACTED ARTICLE: EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells

RETRACTED ARTICLE: EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells

Toxicological Implications of Platinum Nanoparticle Exposure: Stimulation of Intracellular Stress, Inflammatory Response, and Akt Signaling In Vitro

Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PM2.5

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