Characterization of a functional NF-kappa B site in the human interleukin 1 beta 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

Cited by 543 publications

(367 citation statements)

References 69 publications

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“…Upon its activation, NF-κB will translocate to the nucleus to promote expression of stress-inducible genes that can be either pro-or anti-apoptotic, depending on cell system and stimuli [62,63,64,65]. For instance, NF-κB binding sites have been found in the promoter regions of pro-apoptotic genes like inducible nitric oxide synthase [66], cytokines [67], fas and fas-ligand [68]. Examples of anti-apoptotic proteins whose expression is increased by NF-κB are: caspase inhibitors IAP-1, IAP-2 and XIAP [49], mitochondria membrane stabilisers such as Bcl-2 [50], Bcl-xl and Bfl-1 [69], and cell-cycle regulatory proteins like cyclin D1 [70,71].…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 prevents beta cell glucolipotoxicity

et al. 2004

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Aims/hypothesis. We have provided evidence that glucagon-like peptide-1, a potential therapeutic agent in the treatment of diabetes, activates phosphatidylinositol-3 kinase/protein kinase B signalling in the pancreatic beta cell. Since this pathway promotes cell survival in a variety of systems, we tested whether glucagon-like peptide-1 protects beta cells against cell death induced by elevated glucose and/or non-esterified fatty acids. Methods. Human islets and INS832/13 cells were cultured at glucose concentrations of 5 or 25 mmol/l in the presence or absence of palmitate. Apoptosis was evaluated by monitoring DNA fragmentation and chromatin condensation. Wild-type and protein kinase B mutants were overexpressed in INS832/13 cells using adenoviruses. Nuclear factor-κB DNA binding was assayed by electrophoretic mobility shift assay. Results. In human pancreatic beta cells and INS832/13 cells, glucagon-like peptide-1 prevented beta cell apoptosis induced by elevated concentrations of (i) glucose (glucotoxicity), (ii) palmitate (lipotoxicity) and (iii) both glucose and palmitate (glucolipotoxicity). Overexpression of a dominant-negative protein kinase B suppressed the anti-apoptotic action of glucagonlike peptide-1 in INS832/13 cells, whereas a constitutively active protein kinase B prevented beta cell apoptosis induced by elevated glucose and palmitate. Glucagon-like peptide-1 enhanced nuclear factor-κB DNA binding activity and stimulated the expression of inhibitor of apoptosis protein-2 and Bcl-2, two antiapoptotic genes under the control of nuclear factor-κB. Inhibition of nuclear factor-κB by BAY 11-7082 abolished the prevention of glucolipotoxicity by glucagon-like peptide-1. Conclusions/interpretation. The results demonstrate a potent protective effect of glucagon-like peptide-1 on beta cell gluco-, lipo-and glucolipotoxicity. This effect is mediated via protein kinase B activation and possibly its downstream target nuclear factor-κB.

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Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 prevents beta cell glucolipotoxicity

et al. 2004

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“…have been described in the proximal promoter regions of cytokine genes such as MIP-2, TNF-c~, IL-8, GM-CSF, MGSA/ GRO, MIP-I~ and IL-6 genes, and appear to be important in regulating their transcription [21][22][23][24][25][26]. More recently, with the identification and cloning of the CINC gene, an NF-xB motif has also been described in the upstream region, and no other cis-acting regulatory elements were identified on up to 1 kb upstream region that has been cloned [10].…”

Section: Discussionmentioning

confidence: 99%

Ozone induction of cytokine‐induced neutrophil chemoattractant (CINC) and nuclear factor‐κb in rat lung: inhibition by corticosteroids

et al. 1996

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We determined in rat lung whether ozone exposure was associated with the expression of the chemokine, cytokineinduced neutrophil chemoattractant (CINC), and of the transcription factor, NF-~cB. CINC mRNA expression peaked at 2 h after cessation of ozone exposure, and returned to basal levels by 24 h. DNA-binding activity of NF-KB showed a marked increase after ozone, maximal at 2 h. Dexamethasone inhibited CINC mRNA and NF-KB expression, together with neutrophilic inflammation. Our data supports the concept that ozone leads to NF-~cB activation which increases CINC mRNA expression. These series of events could lead to neutrophilic inflammation.Key words: Ozone; Chemokine; CINC mRNA; Lung inflammation; NF-xB Norway rat lung. Recent cloning and sequencing of the CINC gene has shown a binding site for the transcription regulating factor, nuclear factor-xB in its promoter region [12]. To determine whether any increase in CINC transcription was associated with the activation of NF-xB-binding to the CINC promoter, we examined NF-~cB-binding activity to nuclear extracts purified from rat lung after exposure to ozone. To examine further the association of NF-xB-binding and CINC expression, we studied the effect of corticosteroid treatment on these parameters. Because activated glucocorticoid receptors are known to prevent NF-lcB-binding [13], we also studied whether corticosteroids could inhibit both NF-xB-binding and CINC expression, in addition to neutrophilic inflammation, following ozone exposure.

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“…The phosphorylation of MAPK is associated with the subsequent activation of transcription factors, including NF-jB, which plays a critical role in monocyte inflammatory cytokine production after exposure to bacterial stimuli [14][15][16]. Therefore, we further examined the effect of ginsan on NF-jB activation.…”

Section: Ginsan Inhibits S Aureus-induced Nf-jb and Mapk Activationmentioning

confidence: 99%

The immunomodulator ginsan induces resistance to experimental sepsis by inhibiting Toll‐like receptor‐mediated inflammatory signals

et al. 2005

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Ginsan, a polysaccharide extracted from Panax ginseng, has multiple immunomodulatory effects. In this study, we show that pretreatment of ginsan (25 lg/kg) protected mice from lethality induced by Staphylococcus aureus challenge. This survival benefit was associated with enhanced bacterial clearance from circulation, spleen and kidney. The phagocytic activity of macrophages treated with ginsan was significantly enhanced against S. aureus. However, the production of proinflammatory cytokines, such as TNFa, IL-1b, IL-6, IFN-c, IL-12, and IL-18, was markedly down-regulated in ginsan-treated mice compared with those of control-infected mice. The expression of Toll-like receptor (TLR) 2 and the adaptor molecule MyD88, which was greatly increased in septic macrophages, was significantly reduced by ginsan treatment in vitro. Similarly, the expression of phospho-JNK1/2, phospho-p38 MAPK, and NF-jB was decreased in the same culture system. These results illustrate that the antiseptic activity of ginsan can be attributed to enhanced bacterial clearance, and reduced proinflammatory cytokines via the TLR signaling pathway.

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Characterization of a functional NF-kappa B site in the human interleukin 1 beta promoter: evidence for a positive autoregulatory loop.

Cited by 543 publications

References 69 publications

Glucagon-like peptide-1 prevents beta cell glucolipotoxicity

Glucagon-like peptide-1 prevents beta cell glucolipotoxicity

Ozone induction of cytokine‐induced neutrophil chemoattractant (CINC) and nuclear factor‐κb in rat lung: inhibition by corticosteroids

The immunomodulator ginsan induces resistance to experimental sepsis by inhibiting Toll‐like receptor‐mediated inflammatory signals

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