Atypical λ/ιPKC Conveys 5-Lipoxygenase/Leukotriene B4-mediated Cross-talk between Phospholipase A2s Regulating NF-κB Activation in Response to Tumor Necrosis Factor-α and Interleukin-1β

Anthonsen, Marit W.; Andersen, Sonja; Solhaug, Anita; Johansen, Berit

doi:10.1074/jbc.m105264200

Cited by 43 publications

(40 citation statements)

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“…Together with the present findings of induction of cPLA 2 expression by ferrous ammonium citrate, they indicate that cPLA 2 could be induced by free radicals. One possibility is that ferrous ammonium citrate-mediated oxidative stress can induced the expression of nuclear factor-kappa B (NF-κB) [34], which is one of the oxidative stress-responsive transcription factors that has been reported to have binding sites on the cPLA 2 promoter, and this binding may induce the expression of cPLA 2 [35][36][37]. The transcription factor, fos is also increased in times of oxidative stress, and increased fos could have bound to the activator protein-1 (AP-1) binding site of cPLA 2 promoter, and induced the expression of cPLA 2 [36].…”

Section: Discussionmentioning

confidence: 99%

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

et al. 2005

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-The present study was carried out to elucidate the effect of a single episode of oxidative stress on pyramidal neurons of the rat hippocampus. A significant increase in the number of neurons that were immunolabeled for the toxic lipid peroxidation product, 4-hydroxynonenal (HNE) was observed in field CA3 of the hippocampus, at 1 day, 7 days and 14 days after intracerebroventricular injection of 1 µL of 5mM ferrous ammonium citrate, compared to ammonium citrate injected controls at these time points. The number of HNE positive cells was fewer at 14 days, compared to 1 day, after ferrous ammonium citrate injection. The changes in HNE imunoreactivity were paralleled by changes in cytoplasmic phospholipase A 2 (cPLA 2 ) labeling in the pyramidal neurons in adjacent sections, suggesting that some of the HNE could have arisen as a result of peroxidation of arachidonic acid that was released by cPLA 2 . Interestingly, despite the HNE and cPLA 2 labeling, no loss of neurons was observed in adjacent Nissl and Fluoro-Jade stained sections. Electron microscopy also showed that the HNE or cPLA 2 labeled cells had features of injured neurons, rather than necrotic neurons. The reduction of HNE immunoreactivity in neurons at 14 days after oxidative injury, and the absence of cell loss at any of the time intervals, shows that hippocampal pyramidal neurons have remarkable ability to recover from a single episode of oxidative stress, if repeated injury such as seizures / excitotoxicity could be avoided.iron / neurodegeneration / 4-hydroxynonenal / cytosolic phospholipase A 2 / lipid peroxidation / antioxidant defenses Abbreviations: AP-1: activator protein-1; CA: cornu ammonis; cPLA 2 : cytosolic phospholipase A 2;

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Section: Discussionmentioning

confidence: 99%

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

et al. 2005

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“…In general, the 5-LOX pathway leads to proliferative and pro-apoptotic effects in various forms of cancer, with exogenous 5-HETE and cysteinyl leukotrienes having up to a fourfold proliferative effect on four different types of breast cancer cell lines [79]. Stimulation of 5-LOX activity was found to arise due to tumour necrosis factor α (TNF-α), interleukin 1β (IL-1β) and histamine signalling, ultimately resulting in ROS-mediated NF-κB activation [80,81]. Furthermore, cancer cell growth was demonstrated in human testicular cancer tissue, where both 5-and 12-LOX were found to promote induction of cell proliferation, an effect which was suppressed upon inhibition of 5-LOX [82].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Inhibition of arachidonic acid metabolism and its implication on cell proliferation and tumour-angiogenesis

Hyde

Missailidis

2009

International Immunopharmacology

143

101

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Lastly, the benefits of dietary omega-3 fatty acids and their mechanisms of action leading to reduced cancer risk and impeded cancer cell growth are mentioned. Finally, a proposal is put forward, suggesting a novel and integrated approach in viewing the molecular mechanisms and complex interactions responsible for the involvement of AA metabolites in carcinogenesis and the protective effects of omega-3 fatty acids in inflammation and tumour prevention.

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“…IL-1b gene expression and protein production are increased in H. pylori infection and reduced with successful eradication (Wang et al, 1999). A myriad of intracellular signals have been suggested to mediate the effects of IL-1b, including activation of mitogenactivated protein kinase (MAPK), release of arachidonic acid, hydrolysis of sphingomyelin, and production of reactive oxygen species (ROS) (Welsh, 1996;Hofmeister et al, 1997;Anthonsen et al, 2001;Wolf et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β stimulates IL-8 expression through MAP kinase and ROS signaling in human gastric carcinoma cells

et al. 2004

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Recent studies have suggested that the expression of interleukin-8 (IL-8) directly correlates with the vascularity of human gastric carcinomas. In this study, the effect of IL-1b on IL-8 expression in human gastric cancer TMK-1 cells and the underlying signal transduction pathways were investigated. IL-1b induced the IL-8 expression in a time-and concentration-dependent manner. IL-1b induced the activation of extracellular signalregulated kinases-1/2 and P38 mitogen-activated protein kinase (MAPK), but not the activation of c-jun aminoterminal kinse and Akt. Specific inhibitors of MEK-1 (PD980590) and P38 MAPK (SB203580) were found to suppress the IL-8 expression and the IL-8 promoter activity. Expression of vectors encoding a mutated-type MEK-1 and P38 MAPK resulted in decrease in the IL-8 promoter activity. IL-1b also induced the production of reactive oxygen species (ROS). N-acetyl cysteine (NAC) prevented the IL-1b-induced ROS production and IL-8 expression. In addition, exogenous H 2 O 2 could induce the IL-8 expression. Deletional and site-directed mutagenesis studies on the IL-8 promoter revealed that activator protein-1 (AP-1) and nuclear factor (NF)-jB sites were required for the IL-1b-induced IL-8 transcription. Electrophoretic mobility shift assay confirmed that IL-1b increased the DNA-binding activity of AP-1 and NF-jB. Inhibitor (PD980590, SB203580) and ROS scavenger (NAC) studies revealed that the upstream signalings for the transcription factors AP-1 and NF-jB were MAPK and ROS, respectively. Conditioned media from the TMK-1 cells pretreated with IL-1b could remarkably stimulate the in vitro growth of HUVEC and this effect was partially abrogated by IL-8-neutralizing antibodies. The above results suggest that MAPK-AP-1 and ROS-NF-jB signaling pathways are involved in the IL-1b-induced IL-8 expression and that these paracrine signaling pathways induce endothelial cell proliferation.

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Atypical λ/ιPKC Conveys 5-Lipoxygenase/Leukotriene B4-mediated Cross-talk between Phospholipase A2s Regulating NF-κB Activation in Response to Tumor Necrosis Factor-α and Interleukin-1β

Abstract: The transcription factor nuclear factor B (NF-B) plays crucial roles in a wide variety of biological functions such as inflammation, stress, and immune responses. We have shown previously that secretory nonpancreatic (

Cited by 43 publications

References 90 publications

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

Injury and recovery of pyramidal neurons in the rat hippocampus after a single episode of oxidative stress induced by intracerebroventricular injection of ferrous ammonium citrate

Inhibition of arachidonic acid metabolism and its implication on cell proliferation and tumour-angiogenesis

Interleukin-1β stimulates IL-8 expression through MAP kinase and ROS signaling in human gastric carcinoma cells

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