Characterization of a Functional NF-κB Site in the Human Interleukin 1β Promoter: Evidence for a Positive Autoregulatory Loop

Hiscott, John; Marois, James J.; Garoufalis, J; D’Addario, Mario; Roulston, Anne; Kwan, I; Pépin, N; Lacoste, Judith; Nguyen, Hannah; Bensi, G

doi:10.1128/mcb.13.10.6231-6240.1993

Cited by 54 publications

(36 citation statements)

References 64 publications

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“…43 Additionally, intestinal epithelial cell-specific deletion of IKKB mark-edly reduced DSS-promoted tumor multiplicity, thereby illustrating the necessity of NF-jB signaling in DSS-promoted tumorigenesis. 43 Activation of the NF-jB signaling pathway has been shown to be responsive to excess ROS and is important in the expression of the proinflammatory cytokines, TNFa, 44,45 IL-1B 46 and IL-6. 47 Therefore, the diminution of oxidative stress by Nrf2regulated antioxidative enzymes resulting in decreased NF-jB activation represents a possible anti-inflammatory mechanism for the attenuated DSS-mediated cytokine expression and accumulation of inflammatory cells seen in colons from WT but not N0 mice.…”

Section: Discussionmentioning

confidence: 99%

Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment

Osburn

Karim

Dolan

et al. 2007

Intl Journal of Cancer

176

118

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Chronic inflammation has been associated with increased risk of developing cancer. The transcription factor NF-E2-related factor 2 (Nrf2) controls the expression of numerous antioxidative enzymes that have been shown to attenuate acute inflammation. The present study investigated the role of Nrf2 genotype in modulating inflammation-promoted colorectal tumorigenesis. Nrf2 wild-type (WT) and Nrf2-deficient (N0) mice were administered a single dose of azoxymethane followed by a 1-week dose of drinking water with or without 1% dextran sulfate sodium (DSS). Aberrant crypt foci were counted 3 weeks after the cessation of DSS treatment. DSS treatment significantly increased numbers of aberrant crypt foci in N0 mice, but not WT mice. The extent of inflammation over the course of DSS treatment was analyzed in both genotypes. Histological analysis of colon sections revealed that N0 mice had markedly increased inflammation and mucosal damage when compared to WT mice beginning on Day 6 of DSS treatment. Although similar levels of inflammatory and oxidative damage biomarkers were evident in colons from WT and N0 mice at the start of DSS treatment, increased colonic proinflammatory cytokine mRNA transcript levels, myeloperoxidase activity and 3-nitrotyrosine immunoreactivity were observed on Day 6 of DSS treatment in N0 mice, but not WT mice. Additionally, DSS treatment resulted in increased lipid peroxidation and loss of aconitase activity in N0 mice, but not WT mice, reflecting increased oxidative damage in colons from N0 mice. Taken together, these results clearly illustrate the role of Nrf2 in regulating an adaptive response that protects against early-phase inflammation-mediated tumorigenesis. ' 2007 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment

Osburn

Karim

Dolan

et al. 2007

Intl Journal of Cancer

176

118

View full text Add to dashboard Cite

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“…Other signal receptors that can activate a noncanonical NF-jB signaling cascade via the NF-jB-inducing kinase (NIK) include lymphotoxin B, B-cell activating factor, CD27, and CD40 [61,62]. Over 300 NF-jB target genes have been confirmed in various roles related to inflammation, including cytokines/ chemokines (IFNG [63], IL-1B [64], IL-6 [65], CCL2 [66], TNFA [67]), immunoreceptors (CD40 [68], TNFR1S1B [69], TLR2 [70], NOD2 [71]), cell adhesion molecules (E-selectin [72], ICAM-1 [73], VCAM-1 [74]), stress response genes (PTGS2 [75], NOS2 [76], SOD2 [77]), growth factors (IGFBP1 [78], VEGFC [79]), and other transcription factors (IRF1 [80], MYC [81], TP53 [82]).…”

Section: Inflammation-linked Signaling Cascades: the Nf-jb And Mapk P...mentioning

confidence: 99%

A tale of two proteins: PACT and PKR and their roles in inflammation

et al. 2021

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“…Of note, NF-κB is a key transcriptional factor for regulating the inflammatory response [ 43 ]. There are a series of studies indicating that NLRP3, IL-1β, and IL-6 are the target genes of NF-κB [ 41 , 44 , 45 ]. Consistently, our data also showed that Bay11-7082, an NF-κB specific inhibitor, reversed the LPS-induced expression of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6, suggesting that NF-κB activation could participate in regulating neuroinflammation.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin suppresses NLRP3 inflammasome activation in intracerebral hemorrhage via TLR4- and MyD88-dependent pathways

Chen

Sui

Cao

et al. 2022

Aging

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Intracerebral hemorrhage (ICH) is a common neurological condition that causes severe disability and even death. Even though the mechanism is not clear, increasing evidence shows the efficacy of atorvastatin on treating ICH. In this study, we examined the impact of atorvastatin on the NOD-like receptor protein 3 (NLRP3) inflammasome and inflammatory pathways following ICH. Mouse models of ICH were established by collagenase injection in adult C57BL/6 mice. IHC mice received atorvastatin treatment 2 h after hematoma establishment. First, the changes of glial cells and neurons in the brains of ICH patients and mice were detected by immunohistochemistry and western blotting. Second, the molecular mechanisms underlying the microglial activation and neuronal loss were evaluated after the application of atorvastatin. Finally, the behavioral deficits of ICH mice without or with the treatment of atorvastatin were determined by neurological defect scores. The results demonstrated that atorvastatin significantly deactivated glial cells by reducing the expression of glial fibrillary acidic protein (GFAP), Ionized calcium binding adapter molecule 1 (Iba1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in ICH model mice. For inflammasomes, atorvastatin also showed its efficacy by decreasing the expression of NLRP3, cleaved caspase-1, and IL-1β in ICH mice. Moreover, atorvastatin markedly inhibited the upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), which indicated deactivation of NLRP3 inflammasomes. By inhibiting the activities of inflammasomes in glial cells, neuronal loss was partially prevented by suppressing the apoptosis in the brains of ICH mice, protecting them from neurological defects.

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Characterization of a Functional NF-κB Site in the Human Interleukin 1β Promoter: Evidence for a Positive Autoregulatory Loop

Cited by 54 publications

References 64 publications

Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment

Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment

A tale of two proteins: PACT and PKR and their roles in inflammation

Atorvastatin suppresses NLRP3 inflammasome activation in intracerebral hemorrhage via TLR4- and MyD88-dependent pathways

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