Search results for "Acinar cell"

showing 8 items of 8 documents

Sjögren's autoimmunity: how perturbation of recognition in endomembrane traffic may provoke pathological recognition at the cell surface

1998

CD4 T cell antigen recognition requires presentation by major histocompatibility complex Class II molecules (MHC II). B cell surface immunoglobulins recognize antigens independently of MHC II, but activation typically requires CD4 cell cytokines as accessory signals. Plasma membrane-endomembrane traffic in lacrimal gland acinar cells, targets of autoimmune activity in Sjogren's syndrome, may satisfy both requirements. The Golgi protein galactosyltransferase and the lysosomal proteins cathepsin B and cathepsin D appear at the plasma membranes during sustained secretomotor stimulation. The RNA transcription termination factor La, a frequent target of Sjogren's autoantibodies, appears in the a…

Cathepsin DLymphocyte proliferationBiologyCathepsin BCell biologymedicine.anatomical_structureAntigenStructural BiologymedicineAcinar cellEndomembrane systemAntigen-presenting cellMolecular BiologyB cellJournal of Molecular Recognition
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In vivo reprogramming for tissue repair.

2015

Berninger and colleagues define milestones for in vivo reprogramming and discuss recent developments in reprogramming into pancreatic b-cells and neurons. Vital organs such as the pancreas and the brain lack the capacity for effective regeneration. To overcome this limitation, an emerging strategy consists of converting resident tissue-specific cells into the cell types that are lost due to disease by a process called in vivo lineage reprogramming. Here we discuss recent breakthroughs in regenerating pancreatic β-cells and neurons from various cell types, and highlight fundamental challenges that need to be overcome for the translation of in vivo lineage reprogramming into therapy.

Cell typeLineage (genetic)Cell- and Tissue-Based TherapyAcinar CellsBiologyIn vivoInsulin-Secreting CellsmedicineHumansRegenerationCell LineagePancreasNeuronsBrain DiseasesRegeneration (biology)BrainPancreatic DiseasesTranslation (biology)Cell DifferentiationCell BiologyTissue repairCellular ReprogrammingCell biologymedicine.anatomical_structurePancreasReprogrammingNeurogliaNature cell biology
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Fibroblast Growth Factor 21 (FGF21) Protects against High Fat Diet Induced Inflammation and Islet Hyperplasia in Pancreas

2015

Fibroblast growth factor 21 (FGF21) is an important endocrine metabolic regulator expressed in multiple tissues including liver and adipose tissue. Although highest levels of expression are in pancreas, little is known about the function of FGF21 in this tissue. In order to understand the physiology of FGF21 in the pancreas, we analyzed its expression and regulation in both acinar and islet tissues. We found that acinar tissue express 20-fold higher levels than that observed in islets. We also observed that pancreatic FGF21 is nutritionally regulated; a marked reduction in FGF21 expression was noted with fasting while obesity is associated with 3–4 fold higher expression. Acinar and islet c…

Male0301 basic medicineFGF21Fibroblast Growth FactorPhysiologyReceptors Antigen T-Cell alpha-betaPeptide Hormoneslcsh:MedicineAdipose tissueAcinar CellsPathology and Laboratory MedicineBiochemistryFatsMiceEndocrinologyMedicine and Health SciencesInsulinlcsh:ScienceImmune ResponseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Multidisciplinarygeography.geographical_feature_categoryFOXP3Forkhead Transcription FactorsFastingHyperplasiaIsletLipidsmedicine.anatomical_structurePhysiological ParametersOrgan SpecificityTumor necrosis factor alphaAnatomymedicine.symptomPancreasSignal TransductionResearch Articlemedicine.medical_specialtyImmunologyEndocrine SystemInflammationBiologyDiet High-FatInterferon-gammaIslets of Langerhans03 medical and health sciencesExocrine GlandsSigns and SymptomsGrowth FactorsInternal medicinemedicineAnimalsObesityPancreasNutritionInflammationDiabetic EndocrinologygeographyHyperplasiaEndocrine PhysiologyTumor Necrosis Factor-alphaBody Weightlcsh:RBiology and Life SciencesGlucagonmedicine.diseaseDietary FatsHormonesDietFibroblast Growth FactorsMice Inbred C57BL030104 developmental biologyEndocrinologyGene Expression RegulationPancreatitisThy-1 Antigenslcsh:QPLOS ONE
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Amylase release from streptolysin O-permeabilized pancreatic acinar cells. Effects of Ca2+, guanosine 5'-[gamma-thio]triphosphate, cyclic AMP, tetanu…

1992

The molecular requirements for amylase release and the intracellular effects of botulinum A toxin and tetanus toxin on amylase release were investigated using rat pancreatic acinar cells permeabilized with streptolysin O. Micromolar concentrations of free Ca2+ evoked amylase release from these cells. Maximal release was observed in the presence of 30 microM free Ca2+. Ca(2+)-stimulated, but not basal, amylase release was enhanced by guanosine 5′-[gamma-thio]triphosphate (GTP[S]) (3-4 fold) or cyclic AMP (1.5-2 fold). Neither the two-chain forms of botulinum A toxin and tetanus toxin, under reducing conditions, nor the light chains of tetanus toxin, inhibited amylase release triggered by Ca2…

MaleBotulinum ToxinsCell Membrane PermeabilityClostridium tetanimedicine.disease_causeBiochemistryNorepinephrineBacterial ProteinsTetanus ToxinAcinar cellmedicineCyclic AMPNeurotoxinAnimalsAmylaseMolecular BiologyPancreasbiologyToxinProteolytic enzymesRats Inbred StrainsCell BiologyRatsBiochemistryGuanosine 5'-O-(3-Thiotriphosphate)AmylasesStreptolysinsbiology.proteinClostridium botulinumStreptolysinCalciumResearch Article
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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Atrial Natriuretic Peptide presence in parotid gland of human fetus at 13th week of development and in adult man

2013

Our immunohistochemical study shows that atrial natriuretic peptide (ANP) is present in both human fetal and adult parotid gland. In the fetuses ANP is localized in cell clusters, while in adult parotid gland, the ANP is seen only in the wall of intra- and extralobular ducts. The results suggest that ANP might play a role in the differentiation of the parotid gland similarly as in brain and that during fetal growth ANP may play a role in the regulating the secretion of primitive salivary fluid, even if acini are still not developed. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 55-58)

Settore BIO/17 - IstologiaAdultMalemedicine.medical_specialtyHistologyGestational AgePeptide hormonePathology and Forensic MedicineFetusstomatognathic systemAtrial natriuretic peptideANPhuman parotid glandontogenyInternal medicineinglesemedicineAcinar cellHumansParotid GlandSecretionFetusSettore BIO/16 - Anatomia Umanabusiness.industryGeneral MedicineParotid glandmedicine.anatomical_structureEndocrinologyHuman fetalcardiovascular systemImmunohistochemistrybusinessAtrial Natriuretic Factorhormones hormone substitutes and hormone antagonistscirculatory and respiratory physiologyFolia Histochemica et Cytobiologica
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Epigenetic Regulation of Early- and Late-Response Genes in Acute Pancreatitis

2015

Abstract Chromatin remodeling seems to regulate the patterns of proinflammatory genes. Our aim was to provide new insights into the epigenetic mechanisms that control transcriptional activation of early- and late-response genes in initiation and development of severe acute pancreatitis as a model of acute inflammation. Chromatin changes were studied by chromatin immunoprecipitation analysis, nucleosome positioning, and determination of histone modifications in promoters of proinflammatory genes in vivo in the course of taurocholate-induced necrotizing pancreatitis in rats and in vitro in rat pancreatic AR42J acinar cells stimulated with taurocholate or TNF-α. Here we show that the upregulat…

Taurocholic AcidTranscriptional Activation0301 basic medicineChromatin ImmunoprecipitationImmunologyAcinar CellsBiologyMethylationChromatin remodelingEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicineHistone methylationAnimalsImmunology and AllergyNucleosomeEpigeneticsPromoter Regions GeneticEarly Growth Response Protein 1Histone AcetyltransferasesInflammationPancreatitis Acute NecrotizingTumor Necrosis Factor-alphaDNA HelicasesNuclear ProteinsAcetylationHistone acetyltransferaseChromatin Assembly and DisassemblyRatsChromatin030104 developmental biologyHistoneGene Expression Regulation030220 oncology & carcinogenesisbiology.proteinCancer researchProtein Processing Post-TranslationalChromatin immunoprecipitationTranscription FactorsThe Journal of Immunology
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Stimulation with carbachol alters endomembrane distribution and plasma membrane expression of intracellular proteins in lacrimal acinar cells.

2000

The events that lead to Sjogren's autoimmune processes in the lacrimal gland remain poorly understood. The acinar cell's responses to acute cholinergic stimulation include release of secretory products across the apical plasma membrane (apm) and a number of processes related to traffic between endomembrane compartments and the basal-lateral plasma membranes (blm), such as recruitment of Na, K-ATPase, accelerated recycling, and accelerated transcytosis of secretory IgA. We tested the hypothesis that stimulation-induced acceleration of endomembrane traffic is accompanied by changes in compartmentation and increased blm expression of proteins that are normally sequestered in endomembrane compa…

medicine.medical_specialtyAcid PhosphataseImmunoblottingGolgi ApparatusStimulationBiologyCholinergic AgonistsCathepsin BCathepsin BCellular and Molecular Neurosciencesymbols.namesakeInternal medicinemedicineAcinar cellAnimalsEndomembrane systemCells Culturedrab5 GTP-Binding ProteinsDifferential centrifugationEnzyme PrecursorsCell MembraneHistocompatibility Antigens Class IIMembrane Proteinsalpha-GlucosidasesGolgi apparatusGalactosyltransferasesCathepsinsSensory SystemsStimulation Chemicalbeta-N-AcetylhexosaminidasesCell biologyOphthalmologyEndocrinologySjogren's SyndromeTranscytosisrab GTP-Binding ProteinssymbolsCarbacholElectrophoresis Polyacrylamide GelFemaleRabbitsSodium-Potassium-Exchanging ATPaseIntracellularExperimental eye research
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