1,721,090 research outputs found
Metabolic reprograming of microglia in the regulation of the innate inflammatory response
Full text linkMicroglia sustain normal brain functions continuously monitoring cerebral parenchyma to detect neuronal activities and alteration of homeostatic processes. The metabolic pathways involved in microglia activity adapt at and contribute to cell phenotypes. While the mitochondrial oxidative phosphorylation is highly efficient in ATP production, glycolysis enables microglia with a faster rate of ATP production, with the generation of intermediates for cell growth and cytokine production. In macrophages, pro-inflammatory stimuli induce a metabolic switch from oxidative phosphorylation to glycolysis, a phenomenon similar to the Warburg effect well characterized in tumor cells. Modification of metabolic functions allows macrophages to properly respond to a changing environment and many evidence suggest that, similarly to macrophages, microglial cells are capable of a plastic use of energy substrates. Neuroinflammation is a common condition in many neurodegenerative diseases and the metabolic reprograming of microglia has been reported in neurodegeneration. Here we review the existing data on microglia metabolism and the connections with neuroinflammatory diseases, highlighting how metabolic changes contribute to module the homeostatic functions of microglia
Non-neoplastic astrocytes. Key players for brain tumor progression
Full text linkAstrocytes are highly plastic cells whose activity is essential to maintain the cerebral homeostasis, regulating synaptogenesis and synaptic transmission, vascular and metabolic functions, ions, neuro- and gliotransmitters concentrations. In pathological conditions, astrocytes may undergo transient or long-lasting molecular and functional changes that contribute to disease resolutionor exacerbation. In recent years, many studies demonstrated that non-neoplastic astrocytes are key cells of the tumor microenvironment that contribute to the pathogenesis of glioblastoma, the most common primary malignant brain tumor and of secondary metastatic brain tumors.This Mini Review covers the recent development of research on non-neoplastic astrocytes as tumor-modulators. Their double-edged capability to promote cancer progression or to represent potential tools to counteract brain tumors will be discussed
Editorial: The effects of enriched environment on NK cells and macrophages and their underlying mechanisms
No full textThere are two types of stress, namely distress and eustress. An enriched environment (EE) as a model of eustress has been studied mainly in the field of neuroscience, but EE has also recently been studied in the field of immunology and cancer research. Since EE affects various immune cells, including NK cells and macrophages, we called for papers to shed light on such cells and their interactions. Four review articles and two original papers were published. Here, we introduce each manuscript briefly and connect them
Effects of perphenazine on the metabolism of inositol phospholipids in SK-N-BE(2) human neuroblastoma cells
No full textAdministration of myo-[3H]inositol to SK-N-BE(2) human neuroblastoma cells for 24 hr resulted in equilibrium labelling of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP) and phosphatidylinositol 4,5-bisphosphate (PIP2), as well as in retention of a large intracellular pool of free myo-[3H]inositol. Equilibrium labelling was no longer observed when cells were treated for 2 hr with 20 μM perphenazine (PPZ) in label-free medium; under these conditions, myo-[3H]inositol from the retained intracellular pool was incorporated into PI and PIP but not into PIP2. Analysis of water-soluble myo-[3H]inositol derivatives and inositol 1,4,5-trisphosphate mass determination indicated that PPZ did not stimulate phosphoinositide hydrolysis by phospholipase C. These results indicate that PPZ raises PI and PIP levels, whereas it is ineffective in expanding the PIP2 pool. The latter effect is not due to a concomitant synthesis and hydrolysis of this lipid
Pertussis toxin effect on carbachol-elicited stimulation of phosphoinositide hydrolysis in human neuroblastoma [SK-N-BE(2)]
No full textCharbachol (Cch) dose-dependently elicited accumulation of [3H]inositol phosphates (IPs) in human neuroblastoma cells SK-N-BE(2) prelabelled with [3H]myo-inositol and stimulated in the presence of 10 mM Li+. Cell response was observed at agonist concentrations higher than 10-6 M and was nearly maximal at 10-3 M; Cch concentration eliciting half- maximal stimulation of [3H]IPs production was about 3.3 x 10-5 M. Pirenzepine (PZ) inhibited [3H]IPs production, as elicited by 1 mM CCh in the presence of 10 mM Li+, in the concentration range 10-8 -10-4 M, with half maximal effect at 2.5 x 10-7 M. Cell treatment with pertussis toxin (PTX) (100 ng/ml for 6 h) resulted in a 20% reduction of total [3H]IPs accumulation elicited by cell stimulation with 1 mM Cch. Results indicate that the human neuroblastoma cell line SK-N-BE(2) possesses a population of muscarinic receptors, highly sensitive to PZ and coupled to stimulation of phosphoinositide hydrolysis through a mechanism which is only partially sensitive to PTX
Muscarinic stimulation of SK-N-BE(2) human neuroblastoma cells elicits phosphoinositide and phosphatidylcholine hydrolysis: relationship to diacylglycerol and phosphatidic acid accumulation.
Full text linkCALCIUM-ACTIVATED POTASSIUM CHANNELS: A POSSIBLE TARGET FOR THE PHARMACOLOGICAL TREATMENT OF GLIOBLASTOMA
No full textCALCIUM-ACTIVATED POTASSIUM CHANNELS: A POSSIBLE TARGET FOR THE PHARMACOLOGICAL TREATMENT OF GLIOBLASTOMA
No full textEffects of a-difluoromethylornithine treatment on arachidonic acid incorporation into SK-N-BE human neuroblastoma cells
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