Search results for "senescence."

showing 10 items of 335 documents

Echinodermata: The complex immune system in echinoderms

2018

View references (418) The Echinodermata are an ancient phylum of benthic marine invertebrates with a dispersal-stage planktonic larva. These animals have innate immune systems characterized initially by clearance of foreign particles, including microbes, from the body cavity of both larvae and adults, and allograft tissue rejection in adults. Immune responsiveness is mediated by a variety of adult coelomocytes and larval mesenchyme cells. Echinoderm diseases from a range of pathogens can lead to mass die-offs and impact aquaculture, but some individuals can recover. Genome sequences of several echinoderms have identified genes with immune function, including expanded families of Toll-like r…

0301 basic medicineImmunoglobulin geneProteomicsSea CucumbersAntimicrobial peptidesDiseasesImmune responsesBiologySenescenceImmune development03 medical and health sciences0302 clinical medicineImmune systemAsteroideaAsteroidea Brittle stars Coelomocytes Crinoidea Diseases Echinoidea Genomics Holothuroidea Immune development Immune responses Immuno-toxicology Larval immune cells Ophiuroidea Proteomics Sea cucumbers Sea lilies Sea stars Sea urchins SenescenceApostichopus JaponicusSea cucumbersAsteroidea; Brittle stars; Coelomocytes; Crinoidea; Diseases; Echinoidea; Genomics; Holothuroidea; Immune development; Immune responses; Immuno-toxicology; Larval immune cells; Ophiuroidea; Proteomics; Sea cucumbers; Sea lilies; Sea stars; Sea urchins; SenescenceCrinoideaSea starsHolothuroideaOphiuroideaSea urchinsInnate immune systemCoelomocytesfungiLarval immune cellsSea liliesChemotaxisEchinoideaMarine invertebratesGenomicsbiology.organism_classificationComplement systemCell biology030104 developmental biologyEchinodermBrittle starsCoelomocytes Apostichopus Japonicus Sea CucumbersImmuno-toxicology030217 neurology & neurosurgery
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MUC4 is overexpressed in idiopathic pulmonary fibrosis and collaborates with transforming growth factor β inducing fibrotic responses.

2021

Several mucins are implicated in idiopathic pulmonary fibrosis (IPF); however, there is no evidence regarding the role of MUC4 in the development of IPF. Here we demonstrated that MUC4 was overexpressed in IPF patients (n = 22) compared with healthy subjects (n = 21) and located in pulmonary arteries, bronchial epithelial cells, fibroblasts, and hyperplastic alveolar type II cells. Decreased expression of MUC4 using siRNA–MUC4 inhibited the mesenchymal/myofibroblast transformations of alveolar type II A549 cells and lung fibroblasts, as well as cell senescence and fibroblast proliferation induced by TGF-β1. The induction of the overexpression of MUC4 increased the effects of TGF-β1 on mesen…

0301 basic medicineImmunologyCellRespiratory Mucosa03 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicineTransforming Growth Factor betaImmunology and AllergyMedicineHumansMolecular Targeted TherapySmad3 ProteinRNA Small InterferingFibroblastLungCellular SenescenceA549 cellLungMucin-4business.industryMesenchymal stem cellrespiratory systemFibroblastsmedicine.diseaseIdiopathic Pulmonary Fibrosisrespiratory tract diseasesUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureA549 CellsCancer researchsense organsbusinessMyofibroblast030215 immunologyTransforming growth factorSignal TransductionMucosal immunology
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Interactions between immune challenges and cancer cells proliferation: timing does matter!

2015

Using first a theoretical framework, we show that repeated short immune challenges could impact the accumulation of cancerous cells through continuous perturbation of immune system efficiency. We discuss for a new indirect role for infectious disease in cancer progression.

0301 basic medicineMALADIEHealth Toxicology and Mutagenesismedicine.medical_treatmentMedicine (miscellaneous)[SDV.CAN]Life Sciences [q-bio]/CancerBiologyinfectious diseases[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciences0302 clinical medicineImmune systemINFECTIONEpidemiology of cancermedicinecancer[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyOriginal Research ArticleEcology Evolution Behavior and SystematicsIMMUNITEMODELE MATHEMATIQUEimmunosenescenceimmunosuppressionCancerImmunosuppressionImmunosenescencePREVENTION SANITAIREbiochemical phenomena metabolism and nutritionmedicine.diseaseCANCER3. Good health030104 developmental biologyCancer incidence13. Climate action030220 oncology & carcinogenesisImmunologyCancer cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyCancer riskAGENT PATHOGENE
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A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells

2016

Phosphatase and tensin homolog (PTEN) gene is considered a tumor suppressor gene. However, PTEN mutations rarely occur in hepatocellular carcinoma (HCC), whereas heterozygosity of PTEN, resulting in reduced PTEN expression, has been observed in 32–44% of HCC patients. In the present study, we investigated the effects of the small molecule PTEN inhibitor VO-OHpic in HCC cells. VO-OHpic inhibited cell viability, cell proliferation and colony formation, and induced senescence-associated β-galactosidase activity in Hep3B (low PTEN expression) and to a lesser extent in PLC/PRF/5 (high PTEN expression) cells, but not in PTEN-negative SNU475 cells. VO-OHpic synergistically inhibited cell viability…

0301 basic medicineMAPK/ERK pathwayPTENCarcinoma HepatocellularsenescenceTumor suppressor geneCell SurvivalMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineReportOrganometallic CompoundsAnimalsHumansPTENTensinViability assayHCCProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationbiologyCell growthTOR Serine-Threonine KinasesAKTLiver NeoplasmsPTEN PhosphohydrolaseCell BiologySorafenibXenograft Model Antitumor Assaysdigestive system diseasesVO-OHpicGene Expression Regulation Neoplastic030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchSignal TransductionDevelopmental Biology
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p38α regulates actin cytoskeleton and cytokinesis in hepatocytes during development and aging.

2017

[Background]: Hepatocyte poliploidization is an age-dependent process, being cytokinesis failure the main mechanism of polyploid hepatocyte formation. Our aim was to study the role of p38α MAPK in the regulation of actin cytoskeleton and cytokinesis in hepatocytes during development and aging. [Methods]: Wild type and p38α liver-specific knock out mice at different ages (after weaning, adults and old) were used. [Results]: We show that p38α MAPK deficiency induces actin disassembly upon aging and also cytokinesis failure leading to enhanced binucleation. Although the steady state levels of cyclin D1 in wild type and p38α knock out old livers remained unaffected, cyclin B1- a marker for G2/M…

0301 basic medicineMaleAgingRHOAPhysiologylcsh:MedicineArp2/3 complexBiochemistryMitogen-Activated Protein Kinase 14Gene Knockout TechniquesMice0302 clinical medicineContractile ProteinsAnimal CellsMedicine and Health SciencesSmall interfering RNAsCell Cycle and Cell DivisionPost-Translational ModificationPhosphorylationlcsh:ScienceCytoskeletonCyclin B1Cells CulturedCellular SenescenceCytoskeletonMice KnockoutMultidisciplinarybiologyChemistryImmunohistochemistry3. Good healthCell biologyNucleic acidsLiverCell Processes030220 oncology & carcinogenesisCellular TypesAnatomyCellular Structures and OrganellesProtein BindingResearch ArticleMitosismacromolecular substancesProtein Serine-Threonine Kinases03 medical and health sciencesHsp27CyclinsGeneticsAnimalsNon-coding RNAActinCytokinesislcsh:RBiology and Life SciencesProteinsCell BiologyActin cytoskeletonActinsGene regulationCytoskeletal Proteins030104 developmental biologybiology.proteinHepatocytesRNAlcsh:QGene expressionProtein MultimerizationPhysiological ProcessesOrganism DevelopmentCytokinesisBiomarkersDevelopmental BiologyPloS one
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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Synaptic Regulator α-Synuclein in Dopaminergic Fibers Is Essentially Required for the Maintenance of Subependymal Neural Stem Cells.

2018

Synaptic protein -synuclein (-SYN) modulates neurotransmission in a complex and poorly understood manner and aggregates in the cytoplasm of degenerating neurons in Parkinsons disease. Here, we report that -SYN present in dopaminergic nigral afferents is essential for the normal cycling and maintenance of neural stem cells (NSCs) in the brain subependymal zone of adult male and female mice. We also showthat premature senescence of adult NSCs into non-neurogenic astrocytes in mice lacking-SYN resemblesthe effects of dopaminergic fiber degeneration resulting from chronic exposure to 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine or intranigral inoculation of aggregated toxic -SYN. Interestingly…

0301 basic medicineMaleanimal diseases[SDV]Life Sciences [q-bio]DopamineNeurogenesisRegulatorniche biologyBiologyNeurotransmissionenvironment and public health03 medical and health scienceschemistry.chemical_compoundstemnessMice0302 clinical medicineNeural Stem CellsDopaminemedicineSubependymal zoneAnimalsHumansheterocyclic compoundsNeurons AfferentStem Cell NicheResearch ArticlesparkinsonismCellular SenescenceGeneral NeuroscienceMPTPDopaminergic NeuronsNeurogenesisDopaminergicBrainNeural stem cellMice Mutant Strains3. Good healthnervous system diseases[SDV] Life Sciences [q-bio]adult neurogenesis030104 developmental biologychemistrynervous systemalpha-SynucleinFemaleNeuroscience030217 neurology & neurosurgerySnca knock-outmedicine.drug
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Age reduces resistance and tolerance in malaria-infected mice.

2021

7 pages; International audience; Once infected, hosts can rely on two strategies to cope with parasites: fight them (resist the infection) or minimize the damage they induce (tolerate the infection). While there is evidence that aging reduces resistance, how tolerance varies as hosts become old has been barely studied. Here, we used a rodent malaria parasite (Plasmodium yoelii) to investigate whether 2- and 12-month old house mice differ in their capacity to resist and tolerate the infection. We found that 12-month old mice harbored higher parasitemia, showing that age reduces resistance to malaria. Infection-induced deterioration of host health was assessed using red blood cell and body ma…

0301 basic medicineMicrobiology (medical)SenescenceAgingsenescenceRodentAnemia[SDV]Life Sciences [q-bio]030106 microbiologyParasitemiaBiologyParasitemiaMicrobiologyHost-Parasite Interactions03 medical and health sciencesMiceImmunitybiology.animalparasitic diseasesGeneticsmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyMolecular BiologyEcology Evolution Behavior and SystematicsPhysiological PhenomenaDisease ResistanceAge FactorsImmunityPlasmodium yoeliimedicine.diseasebiology.organism_classificationanemia3. Good healthMalaria[SDV] Life Sciences [q-bio]virulenceMice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunology[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleHouse miceDisease SusceptibilityMalariaPlasmodium yoeliiInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside rev…

2019

The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-pa…

0301 basic medicineSenescenceAdultMaleAnti-HIV Agents030106 microbiologyDown-RegulationInflammationHIV InfectionsCCL2Peripheral blood mononuclear cell03 medical and health sciencesVirologyAntiretroviral Therapy Highly ActivePlasminogen Activator Inhibitor 1medicineCXCL10HumansCellular SenescencePharmacologyInflammationbusiness.industryInterleukin-6Interleukin-18virus diseasesMiddle AgedCCL20Chemokine CXCL10030104 developmental biologyInsulin-Like Growth Factor Binding Protein 3ImmunologyLeukocytes MononuclearReverse Transcriptase InhibitorsInterleukin 18Tumor necrosis factor alphaFemalemedicine.symptomTumor Suppressor Protein p53businessAntiviral research
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