Search results for "Receptor Cross-Talk"

showing 5 items of 15 documents

Cholesterol and Amyloid-β: Evidence for a Cross-Talk between Astrocytes and Neuronal Cells.

2011

Accumulating data supports the concept that alterations of cholesterol metabolism might influence the development of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive accumulation of amyloid-β (Aβ) peptides in the brain. Changes in the neuronal production of Aβ have been described as a function of cholesterol levels, thus suggesting a causal link between cholesterol homeostasis dysregulation and AD pathogenesis. Under physiological conditions, cholesterol uptake in the brain is efficiently prevented by the blood-brain barrier, and mature neurons are thought to rely on glial cells for their cholesterol supply. In the present study, we tested the hypothesis t…

Genetically modified mouseBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicCell LinePathogenesisMicechemistry.chemical_compoundAlzheimer DiseasemedicineAnimalsHomeostasisHumansBrain ChemistryNeuronsAmyloid beta-PeptidesbiologyCholesterolGeneral NeuroscienceTransporterReceptor Cross-TalkGeneral Medicinemedicine.diseaseCoculture TechniquesPsychiatry and Mental healthClinical PsychologyCholesterolATP Binding Cassette Transporter 1chemistryAstrocytesABCA1biology.proteinATP-Binding Cassette Transporterslipids (amino acids peptides and proteins)Geriatrics and GerontologyAlzheimer's diseaseNeuroscienceHomeostasisATP Binding Cassette Transporter 1
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Cross-talk between minimally primed HL-60 cells and resting HUVEC reveals a crucial role for adhesion over extracellularly released oxidants

2011

This study demonstrates that a long-lasting co-culture of neutrophil surrogates (HL-60 cells), minimally primed by platelet activating factor (PAF), and resting endothelial cells (EC) results in the elaboration of an hyper-adhesive endothelial surface, as measured by the increase in the expression of endothelial adhesion molecules E-Selectin, VCAM-1, and ICAM-1. This endothelial dysfunction is mediated by the activation of the redox-sensitive transcription factor NF-κB through an exclusive adhesion-driven mechanism active in the endothelial cell: reactive oxygen and nitrogen species, extracellularly released by minimally primed HL-60 cells, are not involved in the induction of the endotheli…

Intercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1HL-60 CellsInflammationNeutrophils Priming Endothelial cells Inflammation Adhesion Oxidants.BiologyBiochemistryCell Linechemistry.chemical_compoundSettore BIO/10 - BiochimicaE-selectinCell AdhesionmedicineHumansEndothelial dysfunctionCell adhesionPharmacologyPlatelet-activating factorCell adhesion moleculeNF-kappa BEndothelial CellsReceptor Cross-TalkIntercellular Adhesion Molecule-1Oxidantsmedicine.diseaseCoculture TechniquesCell biologyEndothelial stem cellchemistrybiology.proteinmedicine.symptomE-SelectinReactive Oxygen SpeciesBiochemical Pharmacology
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Leptin/HER2 crosstalk in breast cancer: in vitro study and preliminary in vivo analysis.

2008

Abstract Background Obesity in postmenopausal women is associated with increased breast cancer risk, development of more aggressive tumors and resistance to certain anti-breast cancer treatments. Some of these effects might be mediated by obesity hormone leptin, acting independently or modulating other signaling pathways. Here we focused on the link between leptin and HER2. We tested if HER2 and the leptin receptor (ObR) can be coexpressed in breast cancer cell models, whether these two receptors can physically interact, and whether leptin can transactivate HER2. Next, we studied if leptin/ObR can coexist with HER2 in breast cancer tissues, and if presence of these two systems correlates wi…

LeptinTranscriptional Activationmedicine.medical_specialtyCancer ResearchReceptor ErbB-2Breast Neoplasmslcsh:RC254-282Breast cancerSurgical oncologyRisk FactorsInternal medicineCell Line TumormedicineGeneticsHumansObesityReceptorskin and connective tissue diseasesneoplasmsLeptin receptorbusiness.industryLeptinCarcinoma Ductal BreastReceptor Cross-Talklcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticPostmenopauseEndocrinologyOncologyImmunohistochemistryReceptors LeptinFemaleSignal transductionbusinessImmunostainingProtein BindingResearch ArticleBMC cancer
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Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2

2012

We investigated the potential anorectic action of peripherally administered glucagon-like peptide 2 (GLP2) in lean and diet-induced obese (DIO) mice. Mice, fasted for 16 h, were injected i.p. with native GLP2 or [Gly2]GLP2, stable analog of GLP2, before or after GLP2 (3–33), a GLP2 receptor (GLP2R) antagonist, or exendin (9–39), a GLP1R antagonist. Food intake was measured at intervals 1, 2, 4, 8, and 24 h postinjection. In addition, we tested in lean mice the influence of [Gly2]GLP2 on gastric emptying and the effects of GLP1 alone or in combination with [Gly2]GLP2 on food intake. [Gly2]GLP2 dose dependently and significantly inhibited food intake in lean and DIO mice. The reduction of foo…

Malemedicine.medical_specialtyTime FactorsEndocrinology Diabetes and MetabolismPeptideDiet High-FatSettore BIO/09 - FisiologiaGlucagon-Like Peptide-1 ReceptorEatingMiceEndocrinologyGLP-2 food intake diet induced obesityGlucagon-Like Peptide 1Internal medicineAppetite DepressantsGlucagon-Like Peptide 2Receptors GlucagonmedicineAnimalsObesityReceptorchemistry.chemical_classificationDose-Response Relationship DrugGastric emptyingAntagonistReceptor Cross-TalkGlucagon-like peptide-2Peptide FragmentsMice Inbred C57BLDose–response relationshipEndocrinologyGastric EmptyingchemistryGlucagon-Like Peptide-2 ReceptorAnorecticGlucagon-Like Peptide-2 Receptor
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Inter- and intracellular signaling in amyotrophic lateral sclerosis: role of p38 mitogen-activated protein kinase.

2006

The pathogenetic processes underlying the selective motor neuron degeneration in amyotrophic lateral sclerosis (ALS) are complex and still not completely understood even in the cases of inherited disease caused by mutations in the Cu/Zn superoxide dismutase-dependent (SOD1) gene. Recent evidence supports the view that ALS is not a cell-autonomous disease and that glial-neuron cross-talk, throughout cytokines and other toxic factors like the nitric oxide and superoxide, is a crucial determinant for the induction of motor neuron death. This cell-cell interaction may determine the progression of the disease through processes that are likely independent of the initial trigger and that may conve…

Motor NeuronsCell signalingp38 mitogen-activated protein kinasesSOD1Amyotrophic Lateral SclerosisNeurotoxicityCell CommunicationReceptor Cross-TalkMotor neuronBiologymedicine.diseasep38 Mitogen-Activated Protein Kinasesmedicine.anatomical_structurenervous systemNeurologyMitogen-activated protein kinasemedicinebiology.proteinAnimalsHumansNeurology (clinical)Amyotrophic lateral sclerosisNeuroscienceNeurogliaNeuroinflammation
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