Search results for "Extracellular"

showing 10 items of 1220 documents

Novel GPR120 agonist TUG891 modulates fat taste perception and preference and activates tongue-brain-gut axis in mice

2020

GPR120 is implicated as a lipid receptor in the oro-sensory detection of dietary fatty acids. However, the effects of GPR120 activation on dietary fat intake or obesity are not clearly understood. We investigated to determine whether the binding of TUG891, a novel GPR120 agonist, to lingual GPR120 modulates fat preference in mice. We explored the effects of TUG891 on obesity-related hormones and conducted behavioral choice tests on mice to better understand the physiologic relevance of the action of TUG891. In cultured mouse and human taste bud cells (TBCs), TUG891 induced a rapid increase in Ca2+ by acting on GPR120. A long-chain dietary fatty acid, linoleic acid (LA), also recruited Ca2+ …

Male0301 basic medicineAgonistlinoleic acidmedicine.medical_specialtyTasteextracellular signal-regulated kinase 1/2obesitymedicine.drug_classLinoleic acidQD415-436030204 cardiovascular system & hematologyBiochemistryReceptors G-Protein-CoupledMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyTongueInternal medicinemedicineAnimalsHumansReceptorCells CulturedResearch ArticlesCholecystokininchemistry.chemical_classificationPhenylpropionatesBiphenyl CompoundsBrainTaste PerceptionFatty acidGPR120Cell BiologyTaste BudsGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologychemistryglucagon-like peptide-1Hormone
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Vitronectin as a molecular player of the tumor microenvironment in neuroblastoma

2019

Background Vitronectin is a multifunctional glycoprotein known in several human tumors for its adhesive role in processes such as cell growth, angiogenesis and metastasis. In this study, we examined vitronectin expression in neuroblastoma to investigate whether this molecule takes part in cell-cell or cell-extracellular matrix interactions that may confer mechanical properties to promote tumor aggressiveness. Methods We used immunohistochemistry and image analysis tools to characterize vitronectin expression and to test its prognostic value in 91 neuroblastoma patients. To better understand the effect of vitronectin, we studied its in vitro expression using commercial neuroblastoma cell lin…

Male0301 basic medicineCancer ResearchAngiogenesislcsh:RC254-282MetastasisExtracellular matrixMice03 medical and health sciencesNeuroblastoma0302 clinical medicineCell Line TumorNeuroblastomaImage Interpretation Computer-AssistedTumor MicroenvironmentGeneticsmedicineAnimalsHumansDigital pathologyVitronectinMigrationTumor microenvironmentbiologyCell growthChemistryExtracellular matrixlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosismedicine.diseaseSurvival AnalysisUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchbiology.proteinImmunohistochemistryFemaleVitronectinNeoplasm TransplantationResearch Article
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β1 integrin signaling promotes neuronal migration along vascular scaffolds in the post-stroke brain

2017

Cerebral ischemic stroke is a main cause of chronic disability. However, there is currently no effective treatment to promote recovery from stroke-induced neurological symptoms. Recent studies suggest that after stroke, immature neurons, referred to as neuroblasts, generated in a neurogenic niche, the ventricular-subventricular zone, migrate toward the injured area, where they differentiate into mature neurons. Interventions that increase the number of neuroblasts distributed at and around the lesion facilitate neuronal repair in rodent models for ischemic stroke, suggesting that promoting neuroblast migration in the post-stroke brain could improve efficient neuronal regeneration. To move t…

Male0301 basic medicineChain migrationlcsh:MedicineExtracellular matrixNeural Stem CellsCell MovementLamininCells CulturedMice KnockoutNeuronslcsh:R5-920Mice Inbred ICRMicroscopy ConfocalTissue ScaffoldsbiologyIntegrin beta1BrainCell migrationGeneral MedicineCell biologyStrokeVasculature-guided migrationFemaleBlood vesselmedicine.symptomlcsh:Medicine (General)Signal TransductionResearch Paperanimal structuresIntegrinMice TransgenicGeneral Biochemistry Genetics and Molecular BiologyLesion03 medical and health sciencesNeuroblastβ1 integrinNeuroblast migrationmedicineAnimalsRegeneration (biology)lcsh:RCoculture TechniquesMicroscopy Electron030104 developmental biologynervous systemAstrocytesImmunologybiology.proteinBlood VesselsLamininEBioMedicine
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Extra collagen overlay prolongs the differentiated phenotype in sandwich-cultured rat hepatocytes

2018

INTRODUCTION: Sandwich-cultured rat hepatocytes (SCRH) have become an invaluable in vitro model to study hepatic drug disposition. SCRH are maintained between two layers of extracellular matrix. In this configuration, culture periods of 4days are typically applicable. The aim of the present study was to modify conventional SCRH by applying an additional collagen overlay to prolong the hepatic phenotype in SCRH and thus to extend the applicability of the model. METHODS: The cultures receiving an extra top layer ('SCRH-plus' cultures) were compared with the conventional SCRH by testing the morphology, cell functionality, metabolic capacity and Mrp2-activity. RESULTS: In the SCRH-plus cultures…

Male0301 basic medicineGlucuronosyltransferaseCellular differentiationCellCell Culture TechniquesToxicologyExtracellular matrix03 medical and health sciencesBile canaliculiMethodsmedicineAnimalsBileGlucuronosyltransferaseRats WistarCells CulturedPharmacologybiologyCell DifferentiationMetabolismPhenotypeExtracellular MatrixRatsCell biologyPhenotype030104 developmental biologymedicine.anatomical_structureLiverBiochemistryCell cultureToxicityHepatocytesbiology.proteinHepatic drug dispositionCollagenSandwich-cultured hepatocytesJournal of Pharmacological and Toxicological Methods
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Perineuronal Nets Regulate the Inhibitory Perisomatic Input onto Parvalbumin Interneurons and γ Activity in the Prefrontal Cortex

2020

Parvalbumin-expressing (PV+) interneurons play a key role in the maturation and synchronization of cortical circuitry and alterations in these inhibitory neurons, especially in the medial prefrontal cortex (mPFC), have been found in different psychiatric disorders. The formation of perineuronal nets (PNNs) around many of these interneurons at the end of the critical periods reduces their plasticity and sets their connectivity. Consequently, the presence of PNNs must have an important impact on the synaptic input and the physiology of PV+ cells. In the present study, we have found that in adult male mice, prefrontocortical PV+ cells surrounded by PNNs show higher density of perisomatic excit…

Male0301 basic medicineInterneuronPrefrontal CortexInhibitory postsynaptic potentialMice03 medical and health sciences0302 clinical medicineInterneuronsBasket cellmedicineExtracellularAnimalsGamma RhythmPrefrontal cortexResearch ArticlesNeuronal PlasticitybiologyChemistryGeneral NeurosciencePerineuronal netExtracellular MatrixMice Inbred C57BLParvalbumins030104 developmental biologymedicine.anatomical_structurenervous systembiology.proteinExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryParvalbuminThe Journal of Neuroscience
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Downregulation of intratumoral expression of miR-205, miR-200c and miR-125b in primary human cutaneous melanomas predicts shorter survival

2018

AbstractWhile only 15–25 percent of melanoma patients develop distant metastasis and die, this disease is still responsible for the majority of skin cancer-related deaths. The availability of adjuvant therapies makes the selection of high-risk patients essential. We evaluated the intratumoral expression of ten miRNAs in primary melanomas in relation to its ability to predict melanoma survival. To this end, we correlated miRNA expression in 132 cryopreserved primary and metastatic tumors with clinicopathological factors and clinical outcome. We found sequential downregulation of intratumoral expression of miR-125b, miR-182, miR-200c and miR-205 over the full spectrum of melanoma progression.…

Male0301 basic medicineSkin Neoplasmsmedicine.medical_treatmentlcsh:MedicineDown-RegulationDiseaseArticleMetastasisExtracellular matrix03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementmicroRNABiomarkers TumorTumor Cells CulturedmedicineHumansNeoplasm Invasivenesslcsh:ScienceMelanomaAgedCell ProliferationMultidisciplinarybusiness.industryMelanomalcsh:RPrognosismedicine.diseaseIn vitroGene Expression Regulation NeoplasticSurvival RateMicroRNAs030104 developmental biology030220 oncology & carcinogenesisDisease ProgressionCancer researchlcsh:QFemalebusinessAdjuvantFollow-Up StudiesScientific Reports
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Amelioration of the abnormal phenotype of a new L1 syndrome mouse mutation with L1 mimetics

2021

L1 syndrome is a rare developmental disorder characterized by hydrocephalus of varying severity, intellectual deficits, spasticity of the legs, and adducted thumbs. Therapy is limited to symptomatic relief. Numerous gene mutations in the L1 cell adhesion molecule (L1CAM, hereafter abbreviated L1) were identified in L1 syndrome patients, and those affecting the extracellular domain of this transmembrane type 1 glycoprotein show the most severe phenotypes. Previously analyzed rodent models of the L1 syndrome focused on L1-deficient animals or mouse mutants with abrogated cell surface expression of L1, making it difficult to test L1 function-triggering mimetic compounds with potential therapeu…

Male0301 basic medicineToluidinesL1NeurogenesisCellNeural Cell Adhesion Molecule L1Gene mutationBiologyDuloxetine Hydrochloridemedicine.disease_causeBiochemistryCerebral VentriclesCorpus CallosumMice03 medical and health sciences0302 clinical medicineCerebellumIntellectual DisabilityGeneticsmedicineExtracellularAnimalsL1 syndromeMolecular BiologyCells CulturedNeuronsMutationSpastic Paraplegia HereditaryTrimebutineGenetic Diseases X-LinkedCell migrationSymptomatic reliefMice Inbred C57BLPhenotype030104 developmental biologymedicine.anatomical_structureMutationCancer researchPeptidomimeticsLocomotion030217 neurology & neurosurgeryBiotechnologyThe FASEB Journal
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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Dark exposure affects plasticity-related molecules and interneurons throughout the visual system during adulthood

2020

Several experimental manipulations, including visual deprivation, are able to induce critical period-like plasticity in the visual cortex of adult animals. In this regard, many studies have analyzed the effects of dark exposure in adult animals, but still little is known about the role of interneurons and plasticity-related molecules on such mechanisms. In this study, we analyzed the effects of 10 days of dark exposure on the connectivity and structure of interneurons, both in the primary visual cortex and in the rest of cerebral regions implicated in the transmission of visual stimulus. We found that this environmental manipulation induces changes in the expression of synaptic molecules th…

Male0301 basic medicinegenetic structuresinterneurons ()Mice TransgenicNeural Cell Adhesion Molecule L1Stimulus (physiology)PlasticityInhibitory postsynaptic potentialsensory deprivation ()Mice03 medical and health sciences0302 clinical medicineInterneuronsextracellular matrix ()medicineAnimalsVisual Cortexvisual pathways ()Neuronal PlasticitybiologyGeneral NeurosciencePerineuronal netAge FactorsDarknessPSA-NCAM ()030104 developmental biologyVisual cortexmedicine.anatomical_structureSialic Acidsbiology.proteinNeural cell adhesion moleculeneuronal plasticity ()Nerve NetSensory DeprivationNeuroscience030217 neurology & neurosurgeryParvalbumin
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Deficiency of Plasminogen Activator Inhibitor Type 2 Limits Brain Edema Formation after Traumatic Brain Injury

2019

Plasminogen activator inhibitor-2 (PAI-2/SerpinB2) inhibits extracellular urokinase plasminogen activator (uPA). Under physiological conditions, PAI-2 is expressed at low levels but is rapidly induced by inflammatory triggers. It is a negative regulator of fibrinolysis and serves to stabilize clots. In the present study, PAI-2 expression is upregulated 25-fold in pericontusional brain tissue at 6 h after traumatic brain injury (TBI), with a maximum increase of 87-fold at 12 h. To investigate a potentially detrimental influence of PAI-2 on secondary post-traumatic processes, male PAI-2-deficient (PAI-2-KO) and wild-type mice (WT) were subjected to TBI by controlled cortical impact injury. Br…

Male030506 rehabilitationmedicine.medical_specialtyTraumatic brain injuryBrain EdemaInflammationBlood–brain barrierMice03 medical and health sciences0302 clinical medicineInternal medicineBrain Injuries TraumaticPlasminogen Activator Inhibitor 2medicineExtracellularAnimalsMice KnockoutBrain edemaUrokinase Plasminogen Activatorbusiness.industrymedicine.diseaseMice Inbred C57BLEndocrinologymedicine.anatomical_structureNeurology (clinical)medicine.symptom0305 other medical sciencebusinessPlasminogen activator030217 neurology & neurosurgeryJournal of Neurotrauma
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