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Strana 1 z 1036 Výsledek
Tumor Necrosis Factor-α Suppresses Activation of Sustained Potassium Currents in Rat Small Diameter Sensory Neurons.
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Přihlášení Registrace
Tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine, produces pain and hyperalgesia by activating and/or sensitizing nociceptive sensory neurons. In the present study, using whole-cell patch clamp techniques, the regulation of potassium currents by TNF-α was examined in acutely dissociated
Alterations in macrophage free radical and tumor necrosis factor production by a potassium channel activator.
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The potassium channel activator nicorandil, under evaluation for antianginal management, has been shown to decrease neutrophil respiratory burst. Since our laboratory has demonstrated that reactive oxygen species (ROS) increase tumor necrosis factor (TNF) production, we hypothesized that nicorandil
Angiotensin II and tumour necrosis factor alpha as mediators of ATP-dependent potassium channel remodelling in post-infarction heart failure.
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OBJECTIVE
Angiotensin II (Ang II) and tumour necrosis factor alpha (TNFalpha) are involved in the progression from compensated hypertrophy to heart failure. Here, we test their role in the remodelling of ATP-dependent potassium channel (K(ATP)) in heart failure, conferring increased metabolic and
Effects of tumor necrosis factor on inward potassium current and cell morphology in cultured human oligodendrocytes.
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The effects of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) on inward rectifier potassium [K(IR)] currents and on cell morphology have been studied in cultured human oligodendrocytes. Cell-attached patches were used to isolate and record unitary currents through an inward rectifier K+
Selective opening of mitochondrial ATP-sensitive potassium channels during surgically induced myocardial ischemia decreases necrosis and apoptosis.
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OBJECTIVE
Mitochondrial ATP-sensitive potassium channels have been proposed to be myoprotective. The relevance and specificity of this mechanism in cardiac surgery was unknown. The purpose of this study was to examine the effects of the mitochondrial potassium ATP-sensitive channel opener diazoxide
Tumor necrosis factor enhancement of transient outward potassium currents in cultured rat cortical neurons.
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The effect of recombinant human tumor necrosis factor-alpha (TNF) on voltage-gated membrane currents of cultured neurons derived from embryonic rat cerebral cortex was studied using the whole-cell patch-clamp technique. Treatment of neurons with TNF resulted in an increase in outward potassium
Tumor necrosis factor α modulates sodium-activated potassium channel SLICK in rat dorsal horn neurons via p38 MAPK activation pathway.
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The dorsal horn (DH) of the spinal cord is the integrative center that processes and transmits pain sensation. Abnormal changes in ion channel expression can enhance the excitability of pain-related DH neurons. Sodium-activated potassium (KNa) channels are highly expressed particularly in the
Concomitant induction of apoptosis and necrosis in cerebellar granule cells following serum and potassium withdrawal.
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Serum and potassium withdrawal-induced cell death of cerebellar granule cells is one of the most popular models used for studying neuronal apoptosis in vitro, and it is generally assumed that compounds preventing cell death in this model prevent apoptosis. In the present study we demonstrate that
Metabolic indices related to leaf marginal necrosis associated with potassium deficiency in tomato using GC/MS metabolite profiling
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To clarify the physiological factors associated with the development of tomato leaf marginal necrosis associated with potassium deficiency, tomato leaf blades prior to development of the symptoms were collected, and profiles of water-soluble metabolites were analyzed using gas chromatography-mass
THE INFLUENCE OF DIET UPON NECROSIS CAUSED BY HEPATIC AND RENAL POISONS : PART II. DIET AND THE NEPHRITIS CAUSED BY POTASSIUM CHROMATE, URANIUM NITRATE, OR CHLOROFORM.
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Diet exerts a profound influence upon the toxicity (tested in the omnivorous white rat) of certain substances, namely, chloroform, phosphorus, potassium chromate, and uranium nitrate, which cause necrosis of the parenchymatous cells of the liver or of the kidney. Susceptibility to intoxication with
Tumor necrosis factor-alpha triggers cell death of sensitized potassium chloride-stimulated cholinergic neurons.
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Cell death of cholinergic neurons of the basal forebrain plays an important role in neurodegenerative disorders, such as Alzheimer's disease. Inflammatory cytokines, such as, for example, tumor necrosis factor-alpha (TNF-alpha), may be involved in these neurodegenerative processes. The aim of this
Reduction of potassium currents and phosphatidylinositol 3-kinase-dependent AKT phosphorylation by tumor necrosis factor-(alpha) rescues axotomized retinal ganglion cells from retrograde cell death in vivo.
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Tumor-necrosis-factor-alpha (TNF-alpha) prevented secondary death of retinal ganglion cells (RGCs) after axotomy of the optic nerve in vivo. This RGC rescue was confirmed in vitro in a mixed retinal culture model. In accordance with our previous findings, TNF-alpha decreased outward potassium
Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases.
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Apoptosis is a physiological cell death that culminates in mitochondrial permeability transition and the activation of caspases, a family of cysteine proteases. Necrosis, in contrast, is a pathological cell death characterized by swelling of the cytoplasm and mitochondria and rapid plasma membrane
Activation of potassium and chloride channels by tumor necrosis factor alpha. Role in liver cell death.
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Despite abundant evidence for changes in mitochondrial membrane permeability in tumor necrosis factor (TNF)-mediated cell death, the role of plasma membrane ion channels in this process remains unclear. These studies examine the influence of TNF on ion channel opening and death in a model rat liver
Antibodies against potassium channel interacting protein 2 induce necrosis in isolated rat cardiomyocytes.
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Auto-antibodies against cardiac proteins have been described in patients with dilated cardiomyopathy. Antibodies against the C-terminal part of KChIP2 (anti-KChIP2 [C-12]) enhance cell death of rat cardiomyocytes. The underlying mechanisms are not fully understood. Therefore, we wanted to explore
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