Search results for "Fas Ligand Protein"

showing 10 items of 28 documents

CNS Macrophages Control Neurovascular Development via CD95L.

2017

The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, including the morphogenesis of neurons and vessels. However, whether CNS macrophages can coordinately influence neurovascular development and the identity of the signals involved therein is unclear. Here, we demonstrate that activity of the cell surface receptor CD95 regulates neuronal and vascular morphogenesis in the post-natal brain and retina. Furthermore, we identify CNS macrophages as the main source of CD95L, and macrophage-specific del…

0301 basic medicineFas Ligand ProteinAngiogenesisMorphogenesisvesselmicrogliaBiologyGeneral Biochemistry Genetics and Molecular BiologyRetina03 medical and health sciencesangiogenesisMiceCell surface receptorExtracellularmedicineHuman Umbilical Vein Endothelial CellsNeuritesAnimalsHumansfas Receptorlcsh:QH301-705.5Cell ProliferationRetinaMicrogliaKinaseMacrophagesneurovascular developmentBrainNeurovascular bundle030104 developmental biologymedicine.anatomical_structurecortexsrc-Family Kinasesnervous systemlcsh:Biology (General)ImmunologySynapsesCD95CD95LNeuroscienceCNS macrophagesProtein BindingSignal TransductionCell reports
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Declining Physical Performance Associates with Serum FasL, miR-21, and miR-146a in Aging Sprinters.

2016

Aging is associated with systemic inflammation and cellular apoptosis accelerating physiological dysfunctions. Whether physically active way of life affects these associations is unclear. This study measured the levels of serum inflammatory and apoptotic molecules, their change over 10 years, and their associations with physical performance in sprint-trained male athletes. HsCRP, cell counts, HGB, FasL, miR-21, and miR-146a were measured cross-sectionally (n=67, 18–90 yrs) and serum FasL, miR-21, and miR-146a and their aging-related associations with physical performance were assessed over a 10-year follow-up (n=49, 50–90 yrs). The cross-sectional study showed positive age correlations for …

0301 basic medicineMaleAgingCelllcsh:MedicineSystemic inflammationBench pressFas ligandRunning0302 clinical medicineYoung adultpikajuoksijatAged 80 and overta3141General Medicineinflammatory responseMiddle Agedmedicine.anatomical_structuremedicine.symptomInflammation MediatorsResearch ArticleAdultmedicine.medical_specialtyFas Ligand ProteinArticle SubjectAdolescentGeneral Biochemistry Genetics and Molecular Biologysprinters03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAgedGeneral Immunology and Microbiologybusiness.industryaginglcsh:R030229 sport sciencesphysical performanceCirculating MicroRNAMicroRNAs030104 developmental biologyEndocrinologyCross-Sectional StudiesPhysical performanceApoptosisPhysical FitnessImmunologybusinessBiomarkersFollow-Up StudiesBioMed research international
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Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence…

2011

Abstract Background Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>…

AdultGastritis AtrophicMaleFas Ligand ProteinGenotypeAtrophic gastritisPeptidyl-Dipeptidase AWhite PeopleFas ligandHelicobacter InfectionsRisk FactorsStomach NeoplasmsNod1 Signaling Adaptor ProteinNOD1GenotypemedicineGeneticsHumansGenetics(clinical)fas ReceptorAllelesGenetics (clinical)AgedAged 80 and overPolymorphism GeneticHelicobacter pyloribiologyCancerAngiotensin-converting enzymeMiddle AgedHelicobacter pylorimedicine.diseasebiology.organism_classificationToll-Like Receptor 4ApoptosisImmunologybiology.proteinFemalePrecancerous ConditionsResearch ArticleBMC Medical Genetics
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Involvement of the CD95 (APO-1/Fas) receptor and ligand system in Helicobacter pylori-induced gastric epithelial apoptosis.

1998

Helicobacter pylori infection is associated with chronic gastritis, peptic ulceration, and gastric carcinoma. The potential role of CD95-mediated apoptosis was investigated in a panel of gastric biopsies obtained from patients with H. pylori-associated chronic gastritis (n = 29) and with noninfected normal mucosa (n = 10). Immunohistochemistry revealed increased CD95 receptor expression in epithelial and lamina propria cells in chronic gastritis. By in situ hybridization, CD95 ligand mRNA was absent or low in normal mucosa but expressed at high levels in lamina propria lymphocytes and, unexpectedly, in epithelial cells in chronic gastritis. Apoptotic cells were rare in normal mucosa but wer…

AdultMalePathologymedicine.medical_specialtyFas Ligand ProteinBiopsyReceptor expressionChronic gastritisApoptosisBiologyCell LineHelicobacter InfectionsIn Situ Nick-End LabelingPyloric AntrumTumor Cells CulturedmedicineGastric mucosaHumansCytotoxic T cellRNA Messengerfas ReceptorAgedAged 80 and overLamina propriaMembrane GlycoproteinsHelicobacter pyloriEpithelial CellsGeneral MedicineMiddle AgedHelicobacter pyloriFas receptorbiology.organism_classificationmedicine.diseaseMolecular biologyUp-Regulationmedicine.anatomical_structureGastric MucosaGastritisChronic DiseaseFemaleGastritismedicine.symptomResearch ArticleJournal of Clinical Investigation
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Differential regulation of Fas-mediated apoptosis in both thyrocyte and lymphocyte cellular compartments correlates with opposite phenotypic manifest…

2001

Several mechanisms are probably involved in determining the evolution of autoimmune thyroid disease (AITD) towards either hypothyroidism and the clinical syndrome known as Hashimoto's thyroiditis (HT) or toward hyperthyroidism and the symptoms of Graves' disease (GD). To gain further insight into such mechanisms we performed an exhaustive comparative analysis of the expression of key molecules regulating cell death (Fas, Fas ligand [FasL], Bcl-2) and apoptosis in both thyrocytes and thyroid infiltrating lymphocytes (TILs) from patients with either GD or HT. GD thyrocytes expressed less Fas/FasL than HT thyrocytes, whereas GD TILs had higher levels of Fas/FasL than HT TILs. GD thyrocytes exp…

AdultMaleendocrine systemmedicine.medical_specialtyProgrammed cell deathFas Ligand Proteinendocrine system diseasesEndocrinology Diabetes and MetabolismLymphocyteThyroid Glandchemical and pharmacologic phenomenaApoptosisThyroiditisFas ligandAutoimmune DiseasesEndocrinologyInternal medicinemedicineHumansLymphocytesRNA Messengerfas ReceptorCellular compartmentAgedMembrane GlycoproteinsChemistryReverse Transcriptase Polymerase Chain ReactionThyroidThyroiditis Autoimmunehemic and immune systemsMiddle Agedmedicine.diseasePhenotypeThyroid DiseasesGraves DiseaseEndocrinologymedicine.anatomical_structurePhenotypeGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisFemaleThyroid : official journal of the American Thyroid Association
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Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins

2000

After autoimmune inflammation, interactions between CD95 and its ligand (CD95L) mediate thyrocyte destruction in Hashimoto's thyroiditis (HT). Conversely, thyroid autoimmune processes that lead to Graves' disease (GD) result in autoantibody-mediated thyrotropin receptor stimulation without thyrocyte depletion. We found that GD thyrocytes expressed CD95 and CD95L in a similar manner to HT thyrocytes, but did not undergo CD95-induced apoptosis either in vivo or in vitro. This pattern was due to the differential production of TH1 and TH2 cytokines. Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD …

Adultendocrine systemmedicine.medical_specialtyFas Ligand Proteinendocrine system diseasesCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinThyroid Glandbcl-X ProteinApoptosisMice TransgenicIn Vitro TechniquesThyroiditisThyrotropin receptorMiceTh2 CellsSettore MED/04 - PATOLOGIA GENERALEInternal medicinemedicineImmunology and AllergyAnimalsHumansInterferon gammafas ReceptorInterleukin 4CaspaseMembrane GlycoproteinsbiologyThyroidIntracellular Signaling Peptides and ProteinsThyroiditis AutoimmuneT-Lymphocytes Helper-InducerMiddle AgedTh1 CellsFas receptormedicine.diseaseGraves DiseaseInterleukin 10medicine.anatomical_structureEndocrinologyProto-Oncogene Proteins c-bcl-2biology.proteinCytokinesCarrier Proteinsmedicine.drug
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Resistance to Gemcitabine in a Lymphoma Cell Line Resistant to Fas-mediated Apoptosis

2004

BACKGROUND: The T-cell lymphoma cell line HuT78B1, selected for resistance to Fas-mediated apoptosis, resulted unexpectedly resistant to the apoptotic and cytotoxic effects of gemcitabine (dFdC). We investigated whether this resistance was due to the impairment of the Fas/Fas-ligand (FasL) system. MATERIALS AND METHODS: dFdC effects were studied in HuT78B1 and in the parental Fas-sensitive HuT78 cells exposed to inhibitors of the Fas/FasL system. RESULTS: FasL- and Fas-blocking antibodies did not interfere with dFdC-induced apoptosis in HuT78 cells, whereas inhibitors of caspase-8, -9, -1 or -3 had partial inhibitory effects. Notably, in HuT78B1 cells there was a markedly reduced dFdC accum…

Antimetabolites AntineoplasticFas Ligand ProteinMembrane GlycoproteinsApoptosisLymphoma T-CellCaspase InhibitorsDeoxycytidineGemcitabineEnzyme ActivationLymphoma T-Cell Cell Line Tumor gemcitabineDrug Resistance NeoplasmCaspasesCell Line TumorDeoxycytidine KinaseHumansfas Receptor
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Membrane vesicles shed by oligodendroglioma cells induce neuronal apoptosis.

2006

In order to investigate the mechanism by which oligodendrogliomas cause neuronal damage, media conditioned by G26/24 oligodendroglioma cells, were fractionated into shed vesicles and vesicle-free supernatants, and added to primary cultures of rat fetal cortical neurons. After one night treatment with vesicles, a reproducible, dose-dependent, inhibitory effect on neurite outgrowth was already induced and, after 48-72 h of incubation, neuronal apoptosis was evident. Vesicle-free supernatants and vesicles shed by NIH-3T3 cells had no inhibitory effects on neurons. Western blot analyses showed that treated neurons expressed a decreased amount of neurofilament (NF), growth-associated protein (GA…

Cancer ResearchCell signalingProgrammed cell deathPathologymedicine.medical_specialtyNeurofilamentFas Ligand ProteinNeuriteCellOligodendrogliomaApoptosisCell CommunicationBiologyRats Sprague-DawleyMiceWestern blotmedicineAnimalsMyelin SheathCerebral CortexNeuronsmedicine.diagnostic_testVesicleCytoplasmic Vesiclesoligodendroglioma membrane vesicles neuronal apoptosis Fas-L Nogo.Cell biologyRatsmedicine.anatomical_structureOncologyNIH 3T3 CellsNeuronInternational journal of oncology
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Targeting apoptosis proteins in hematological malignancies

2010

The apoptotic machinery plays a key role in hematopoietic cell homeostasis. Terminally differentiated cells are eliminated, at least in part, by apoptosis, whereas part of the apoptotic machinery, including one or several caspases, is required to go through very specific steps of the differentiation pathways. A number of hematological diseases involve a deregulation of this machinery, which in most cases is a decrease in cell sensitivity to pro-apoptotic signals through over-expression of anti-apoptotic molecules. In some situations however, e.g. in the erythroid lineage of low grade myelodysplastic syndromes, cell sensitivity to apoptosis is increased in a death receptor-dependent manner a…

Cancer ResearchProgrammed cell deathFas Ligand ProteinMyeloidCellular differentiationAmino Acid MotifsAntineoplastic AgentsApoptosisLigandsInhibitor of apoptosisTNF-Related Apoptosis-Inducing LigandCell Line TumormedicineHumansReceptorCaspasebiologyIntrinsic apoptosisCell DifferentiationCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHematologic Neoplasmsbiology.proteinDrug Screening Assays AntitumorApoptosis Regulatory ProteinsSignal TransductionCancer Letters
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