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sphingosine/nécrose
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[Correlation of DNA degradation, induced by tumor necrosis factor-alpha, with accumulation of sphingosine in the nucleus and peroxides in DNA].
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The tumour necrosis factor alpha (TNF-alpha) initiates DNA degradation in many types of cells, eventually resulting in a programmed cell death (apoptosis). In order to study the mechanism of TNF-alpha action in vivo, the dynamics of mouse liver DNA fragmentation was examined after intraperitoneal
Glabridin suppresses intercellular adhesion molecule-1 expression in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells by blocking sphingosine kinase pathway: implications of Akt, extracellular signal-regulated kinase, and nuclear factor-kappaB/Rel signaling pathways.
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(R)-4-(3,4-Dihydro-8,8-dimethyl)-2H,8H-benzo[1,2-b:3,4-b'] dipyran-3yl)-1,3-benzenediol (glabridin) is known to have anti-inflammatory, antimicrobial, and cardiovascular protective activities. In the present study, we report the inhibitory effect of glabridin on intercellular adhesion molecule-1
Effects of tumour necrosis factor-alpha on the coronary circulation of the rat isolated perfused heart: a potential role for thromboxane A2 and sphingosine.
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1. The actions of tumour necrosis factor-alpha (TNF-alpha) on the coronary circulation were investigated in the rat isolated heart, perfused under constant flow, recirculating conditions. 2. An early increase in coronary perfusion pressure (CPP) was observed upon treatment with TNF-alpha (increase
Sphingosine-1-phosphate prevents tumor necrosis factor-{alpha}-mediated monocyte adhesion to aortic endothelium in mice.
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OBJECTIVE
Endothelial activation and monocyte adhesion to endothelium are key events in inflammation. Sphingosine-1-phosphate (S1P) is a sphingolipid that binds to G protein-coupled receptors on endothelial cells (ECs). We examined the role of S1P in modulating endothelial activation and monocyte-EC
Relation of biological activity of mutant forms of recombinant human tumor necrosis factor alpha and accumulation of sphingosine in murine liver.
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TNF-alpha induced sphingomyelin hydrolysis by sphingomyelinase and both sphingosine and ceramide generation have been reported to be implicated in a number of TNF-alpha responses, including cytotoxicity and apoptosis. We found that sphingosine, a highly cytotoxic product of enzymatic degradation of
[The effect of tumor necrosis factor on the free sphingosine level and sphingomyelinase in murine liver cells and nuclei].
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The effects of the human recombinant tumour necrosis factor (TNF) (10 and 40 mg/kg of body mass) on sphingomyelinase activity and sphingosine content in mouse (C57bl) liver cells and nuclei have been studied. Whereas sphingomyelinase is known to be a key enzyme of sphingomyelin metabolism,
Tumor necrosis factor-alpha autoregulates interleukin-6 synthesis via activation of protein kinase C. Function of sphingosine 1-phosphate and phosphatidylcholine-specific phospholipase C.
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We investigated the mechanism of interleukin-6 (IL-6) synthesis induced by tumor necrosis factor-alpha (TNF) in osteoblast-like MC3T3-E1 cells. TNF stimulated the synthesis of IL-6 dose dependently in the range between 1 and 30 ng/ml. Staurosporine and calphostin C, inhibitors of protein kinase C
Tumor necrosis factor-alpha induces stress fiber formation through ceramide production: role of sphingosine kinase.
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Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that activates several signaling cascades. We determined the extent to which ceramide is a second messenger for TNF-alpha-induced signaling leading to cytoskeletal rearrangement in Rat2 fibroblasts. TNF-alpha, sphingomyelinase, or
Tumor necrosis factor-alpha exerts pro-myogenic action in C2C12 myoblasts via sphingosine kinase/S1P2 signaling.
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In this study, we report that low doses of tumor necrosis factor-alpha (TNFalpha) promote myogenesis in C2C12 myoblasts. Moreover, the cytokine increased sphingosine kinase (SphK) activity and induced SphK1 translocation to membranes. The inhibition of SphK functionality by various approaches
Activation of sphingosine kinase by tumor necrosis factor-alpha inhibits apoptosis in human endothelial cells.
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Human umbilical vein endothelial cells (HUVEC), like most normal cells, are resistant to tumor necrosis factor-alpha (TNF)-induced apoptosis in spite of TNF activating sphingomyelinase and generating ceramide, a known inducer of apoptosis. Here we report that TNF activates another key enzyme,
Myocardial dysfunction with coronary microembolization: signal transduction through a sequence of nitric oxide, tumor necrosis factor-alpha, and sphingosine.
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Coronary microembolization results in progressive myocardial dysfunction, with causal involvement of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha uses a signal transduction involving nitric oxide (NO) and/or sphingosine. Therefore, we induced coronary microembolization in anesthetized dogs and
[Correlation of cytotoxic activity of mutant forms of tumor necrosis factor alpha with changes in the level of free sphingosine in murine liver].
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Sphingosine, the product of enzymatic degradation of sphingomyelin, displays a high cytotoxic activity and is accumulated in animal organs under the action of the tumour necrosis factor (TNF alpha). To elucidate the role of sphingosine in the realization of TNF cytotoxicity, TNF mutants were
Sphingosine synergistically stimulates tumor necrosis factor alpha-induced prostaglandin E2 production in human fibroblasts.
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Sphingosine is a biologically active derivative of sphingomyelin. It affects diverse cellular functions and its mechanism(s) of action is poorly defined. Tumor necrosis factor alpha (TNF alpha) has recently been shown to rapidly induce sphingomyelin turnover, implicating this metabolic pathway in
Tumor necrosis factor-alpha-stimulated cell proliferation is mediated through sphingosine kinase-dependent Akt activation and cyclin D expression.
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Tumor necrosis factor-alpha (TNF-alpha) has been shown to activate sphingosine kinase (SphK) in a variety of cell types. The extent to which SphK signaling mediates the pleiotropic effects of TNF-alpha is not entirely clear. The current study examined the role of SphK activity in
Tumor necrosis factor-α-mediated downregulation of the cystic fibrosis transmembrane conductance regulator drives pathological sphingosine-1-phosphate signaling in a mouse model of heart failure.
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BACKGROUND
Sphingosine-1-phosphate (S1P) signaling is a central regulator of resistance artery tone. Therefore, S1P levels need to be tightly controlled through the delicate interplay of its generating enzyme sphingosine kinase 1 and its functional antagonist S1P phosphohydrolase-1. The
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