Search results for "Autophagy"

showing 10 items of 322 documents

Pathogenesis and molecular mechanisms of anderson–fabry disease and possible new molecular addressed therapeutic strategies

2021

Anderson–Fabry disease (AFD) is a rare disease with an incidenceof approximately 1:117,000 male births. Lysosomal accumulation of globotriaosylceramide (Gb3) is the element characterizing Fabry disease due to a hereditary deficiency α-galactosidase A (GLA) enzyme. The accumulation of Gb3 causes lysosomal dysfunction that compromises cell signaling pathways. Deposition of sphingolipids occurs in the autonomic nervous system, dorsal root ganglia, kidney epithelial cells, vascular system cells, and myocardial cells, resulting in organ failure. This manuscript will review the molecular pathogenetic pathways involved in Anderson–Fabry disease and in its organ damage. Some studies reported that i…

ReviewConstriction Pathologicendothelial dysfunctionPathogenesisMicechemistry.chemical_compoundKCa3.1 activitypodocyturiaProtein IsoformsEndothelial dysfunctionBiology (General)SpectroscopyglobotriaosylceramideGlobosidesMicrogliabiologyTOR Serine-Threonine KinasesTrihexosylceramidesmiR-26a-5pGeneral MedicineMitochondriaComputer Science ApplicationsCell biologymiR-152-5pChemistrymedicine.anatomical_structureCerebrovascular CirculationAnderson–Fabry disease Endothelial dysfunction Globotriaosylceramide KCa3.1 activity MiR-1307-5p MiR-152-5p MiR-21-5p MiR-26a-5p Podocyturia Valvular dysfunctionmiR-21-5pSignal TransductionQH301-705.5GlobotriaosylceramideCatalysisInorganic ChemistryAutophagymedicineAnimalsHumansEnzyme Replacement TherapyPhysical and Theoretical ChemistryMolecular BiologyMechanistic target of rapamycinQD1-999PI3K/AKT/mTOR pathwaySphingolipidsAnderson–Fabry diseasebusiness.industryMicrocirculationOrganic ChemistryEndothelial Cellsmedicine.diseaseFabry diseaseSphingolipidMicroRNAschemistrymiR-1307-5palpha-Galactosidasebiology.proteinFabry DiseaseGlycolipidsvalvular dysfunctionLysosomesbusiness
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The YJL185C, YLR376C and YJR129C genes of Saccharomyces cerevisiae are probably involved in regulation of the glyoxylate cycle

2006

The ER24 aci (acidification) mutant of Saccharomyces cerevisiae excreting protons in the absence of glucose was transformed with a multicopy yeast DNA plasmid library. Three different DNA fragments restored the wild-type phenotype termed Aci- because it does not acidify the complete glucose medium under the tested conditions. Molecular dissection of the transforming DNA fragments identified two multicopy suppressor genes YJL185C, YJR129C and one allelic YLR376C. Disruption of either of the three genes in wild-type yeast strain resulted in acidification of the medium (Aci+ phenotype) similarly to the original ER24 mutant. These data indicate the contribution of the ER24 gene product Ylr376Cp…

Saccharomyces cerevisiae ProteinsMutantSaccharomyces cerevisiaeGenes FungalGlyoxylate cycleAutophagy-Related ProteinsGlyoxylatesMethyltransferasesSaccharomyces cerevisiaeBiologyHydrogen-Ion Concentrationbiology.organism_classificationGeneral Biochemistry Genetics and Molecular BiologyYeastCulture MediaGene productchemistry.chemical_compoundPlasmidchemistryBiochemistryGenes SuppressorGeneDNAMetabolic Networks and Pathways
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Resveratrol-induced xenophagy promotes intracellular bacteria clearance in intestinal epithelial cells and macrophages

2019

International audience; Autophagy is a lysosomal degradation process that contributes to host immunity by eliminating invasive pathogens and the modulating inflammatory response. Several infectious and immune disorders are associated with autophagy defects, suggesting that stimulation of autophagy in these diseases should be bene ficial. Here, we show that resveratrol is able to boost xenophagy, a selective form of autophagy that target invasive bacteria. We demonstrated that resveratrol promotes in vitro autophagy-dependent clearance of intracellular bacteria in intestinal epithelial cells and macrophages. These results were validated in vivo using infection in a transgenic GFP-LC3 zebra f…

Salmonella typhimuriumrestrictionResveratrolresveratrolMicechemistry.chemical_compound0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringImmunologieXenophagyImmunology and AllergyIntestinal MucosaZebrafishOriginal Research0303 health sciencessalmonella infectionbiologyChemistrycrohns-disease[SDV.IDA] Life Sciences [q-bio]/Food engineering3. Good healthCell biologyrégime alimentaire030220 oncology & carcinogenesisHost-Pathogen InteractionsAIEClcsh:Immunologic diseases. AllergyautophagysalmonelleTransgenesalmonellaImmunologyautophagieCell Line03 medical and health sciencesImmune systemxenophagyEscherichia coliAnimalsHumans030304 developmental biologyselective autophagyhealthy-volunteersmodelEnterocolitisMacrophagesIntracellular parasiteAutophagylife-span extensionautophagy;resveratrol;xenophagy;salmonella;AIECagent resveratrolEpithelial Cellsbiology.organism_classification[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyCell cultureactivation[SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriologyproteinlcsh:RC581-607Bacteria
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Strategie di difesa attivate in risposta a stress, in embrioni di Paracentrotus lividus

2012

Sea urchin embryos are able to activate different defense strategies against stress. This model system allows to investigate numerous phenomena in multipotent cells, which interact among themselves, in their natural position, bypassing the disadvantages of isolated cells, deprived of their normal network. Cadmium (Cd) treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis. Here we show that Paracentrotus lividus embryos exposed to subacute/sublethal concentrations of Cd adopt autophagy as an additional stratagem to safeg…

Sea Urchin embryos Cadmium autophagy apoptosis stressSettore BIO/06 - Anatomia Comparata E Citologia
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Developmental defects induced by gadolinium ions in sea urchin embryos of phylogenetically distant species

2015

Gadolinium (Gd) is nowadays an emergent environmental pollutant: it is a metal of the lanthanide series of the elements whose chelates are commonly employed as contrast agents for magnetic resonance imaging and subsequently released into the aquatic environment. Sea urchin embryos are highly sensitive to several kinds of stressors and able to activate different defense strategies. The aim of this study was to analyze the consequences of embryo exposure to sublethal Gd concentrations. We compared the effects of Gd on the development of four phylogenetically distant sea urchin species: two Mediterranean species, Paracentrotus lividus and Arbacia lixula, and two species living in the East coas…

Sea UrchinAutophagyApoptosisSettore BIO/06 - Anatomia Comparata E CitologiaSea Urchin; Develpment; Pollution; Autophagy; ApoptosisDevelpmentPollution
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Toxicity induced by Gadolinium ions on sea urchin embryos: comparison among phylogenetically distant species and focus on stress response and skeleto…

2016

Pharmaceuticals are a class of emerging environmental contaminants. Gadolinium (Gd) is a lanthanide metal whose chelates are employed as contrast agents for magnetic resonance imaging, and subsequently released into the aquatic environment. We investigated the effects of exposure to sublethal Gd concentrations on the development of four phylogenetically and geographically distant sea urchin species: two Mediterranean, Paracentrotus lividus and Arbacia lixula, and two from Australia, Heliocidaris tuberculata and Centrostephanus rodgersii. Sensitivity to Gd greatly varied, with EC50 ranging from 56 nM to 132 µM across the four species. Measures of the Gd and Ca content inside embryos showed a…

Sea UrchinGadoliniumEmbyoEmbyo; Ecotoxicology; Gadolinium; Sea UrchinSettore BIO/06 - Anatomia Comparata E CitologiaEcotoxicologygadolinium sea urchin embryo autophagy apoptosis gene expression analysis skeletogenesis
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Autophagy as defence strategy against cadmium stress in Paracentrotus lividus embryos.

2009

Sea urchin embryo is a developmental model that offers an excellent opportunity to investigate the possible adaptive response of cells exposed to different stress during differentiation. These embryos are able to respond to many stress by synthesizing a set of highly conserved proteins, the hsps and/or by activation of apoptosis. The exposure to cadmium trigger the accumulation of metal in embryo cells and the activation of both defence mechanisms depending on concentration and exposure time [1-4]. Recent experimental evidences demonstrate that by autophagy, a highly regulated mechanism that enhances cell survival under various environmental and cellular stress, the breakdown and recycling …

Sea urchin embryo Autophagy CadmiumSettore BIO/06 - Anatomia Comparata E Citologia
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A possible role of autophagy for the execution of apoptosis in cadmium-exposed sea urchin embryos

2012

The sea urchin embryo is a suitable model system that offers an excellent opportunity to investigate different defence strategies activated in stress conditions. We previously showed that cadmium treatment provokes the accumulation of metal in dose- and time-dependent manner in embryonic cells and the activation of defence systems, such as the synthesis of HSPs and/or the initiation of apoptosis. Analysing autophagy, by neutral red, acridine orange and LC3-detection, we demonstrated that Cd-exposed embryos adopt this process as an additional stratagem to safeguard the developmental program. We observed that embryos treated with subletal Cd concentration activate a massive autophagic respons…

Sea urchin autophagy apoptosis cadmium stressSettore BIO/06 - Anatomia Comparata E Citologia
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Sea urchin embryo as a model system for studing autophagy induced by cadmium stress

2010

Sea urchin autophagy cadmium stressSettore BIO/06 - Anatomia Comparata E Citologia
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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