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Sida 1 från 18 resultat
Rapid determination of cell-associated tumor necrosis factor production by flow cytometry.
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BACKGROUND
Tumor necrosis factor (TNF) is a cytokine implicated in many disease states, including septic shock and transplant rejection. Regulation of TNF production is complex, and under certain conditions TNF is expressed in cells, but not released. Determination of TNF, particularly on cells, may
Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent.
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Recent studies suggest that the aryl hydrocarbon receptor (AhR) modulates susceptibilities to some pro-apoptotic agents. AhR-containing murine hepatoma 1c1c7 cultures underwent apoptosis following exposure to tumor necrosis factor-alpha (TNFalpha) + cycloheximide (CHX). In contrast, Tao cells, an
Inhibition of target cell mitochondrial electron transfer by tumor necrosis factor.
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Using digitonin permeabilization to assay mitochondrial electron transfer, we have found that respiratory activity (succinoxidase and cytochrome oxidase) in three mouse fibroblast lines is completely eliminated by incubation with human recombinant tumor necrosis factor-alpha (hrTNF). As with
Reversibility of thiamine deficiency-induced partial necrosis and mitochondrial uncoupling by addition of thiamine to neuroblastoma cell suspensions.
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Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the oxygen consumption decreases and is uncoupled, the mitochondrial cristae are disorganized, the
Thiamine deficiency--induced partial necrosis and mitochondrial uncoupling in neuroblastoma cells are rapidly reversed by addition of thiamine.
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Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled,
Quantitative determination of apoptotic death in cultured human pancreatic cancer cells by propidium iodide and digitonin.
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We present here the efficacy of an in vitro cytotoxicity assay which can measure rapidly both apoptotic dead cells and cell growth rate, quantitatively. Using a multi-well plate reader, the fluorescence intensity of propidium iodide (PI) corresponding to dead cells and to total cells after digitonin
Intrasplenic transplantation of isolated periportal and perivenous hepatocytes as a long-term system for study of liver-specific gene expression.
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Many hepatocyte-specific genes are expressed heterogeneously in the liver lobule depending on the location of the hepatocytes in relation to the inflow or outflow of portal blood (i.e., periportal or perivenous). For example, albumin is expressed in all hepatocytes but more so in the periportal
Molecular mechanisms of gene expression regulation by the apoptosis-promoting protein TIA-1.
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TIA-1 and the related protein TIAR promote DNA fragmentation in digitonin-permeabilized thymocytes. These proteins contain RNA Recognition Motifs (RRMs) and bind uridine-rich sequences. These observations suggested that TIA-1/TIAR are pro-apoptotic factors that influence some aspect of RNA
Zonated expression of cytokines in rat liver: effect of chronic ethanol and the cytochrome P450 2E1 inhibitor, chlormethiazole.
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The release of proinflammatory cytokines by endotoxins and during oxidative stress is considered to be an early key step in the pathogenesis of alcoholic liver disease (ALD). Ethanol-inducible cytochrome P450 2E1 (CYP2E1) has potentially pro-oxidative and toxicological properties, and its expression
Mechanism of Trypanosoma cruzi death induced by Cratylia mollis seed lectin.
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Incubation of T. cruzi epimastigotes with the lectin Cramoll 1,4 in Ca(2+) containing medium led to agglutination and inhibition of cell proliferation. The lectin (50 microg/ml) induced plasma membrane permeabilization followed by Ca(2+) influx and mitochondrial Ca(2+) accumulation, a result that
The mitogen-activated protein kinase pathway can inhibit TRAIL-induced apoptosis by prohibiting association of truncated Bid with mitochondria.
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Breast cancer cells often show increased activity of the mitogen-activated protein kinase (MAPK) pathway. We report here that this pathway reduces their sensitivity to death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and present the underlying mechanism. Activation of
Induction of dystrophin-associated proteins together with nicotinic acetylcholine receptors by denervation in the absence of dystrophin in skeletal muscles of mdx mice.
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We purified the nicotinic acetylcholine receptor from digitonin-solubilized rabbit skeletal muscle by affinity chromatography and detected many proteins linked to AChR, including dystrophin, adhalin, beta-dystroglycan, utrophin, rapsyn, and actin. To determine whether or not AChR links to
BopB is a type III secreted protein in Bordetella bronchiseptica and is required for cytotoxicity against cultured mammalian cells.
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The cytotoxicity of Bordetella bronchiseptica to infected cells is known to be dependent on a B. bronchiseptica type III secretion system. Although the precise mechanism of the type III secretion system is unknown, BopN, BopD and Bsp22 have been identified as type III secreted proteins. In order to
Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes.
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After myocardial ischemia, necrotic cell death occurs mainly during the first minutes of reperfusion through ATP-dependent hypercontracture leading to sarcolemmal rupture. Recent studies indicate that opening of a mitochondrial permeability transition pore (mPTP) is a critical event in
XIAP impairs Smac release from the mitochondria during apoptosis.
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X-linked inhibitor of apoptosis protein (XIAP) is a potent inhibitor of caspases 3, 7 and 9, and mitochondrial Smac (second mitochondria-derived activator of caspase) release during apoptosis inhibits the activity of XIAP. In this study we show that cytosolic XIAP also feeds back to mitochondria to
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