Search results for "Autophagy"

showing 10 items of 322 documents

Ca2+ signalling plays a role in celastrol‐mediated suppression of synovial fibroblasts of rheumatoid arthritis patients and experimental arthritis in…

2019

Background and purpose Celastrol exhibits anti-arthritic effects in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca2+ mobilization in treatment of RA remains undefined. Here, we describe a regulatory role for celastrol-induced Ca2+ signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. Experimental approach We used computational docking, Ca2+ dynamics and functional assays to study the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump (SERCA). In rheumatoid arthritis synovial fibroblasts (RASFs)/rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), mechanisms of Ca2+ -mediated autophagy were analysed by histological, immunohis…

0301 basic medicinemusculoskeletal diseasesMaleProgrammed cell deathSERCAArthritisSarcoplasmic Reticulum Calcium-Transporting ATPasesArthritis RheumatoidRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBAPTAmedicineAutophagyAnimalsHumansCalcium SignalingCells CulturedPharmacologyMice KnockoutGene knockdownbiologyChemistrySynovial MembraneCalpainFibroblastsmedicine.diseaseResearch PapersArthritis ExperimentalTriterpenesCalcineurin030104 developmental biologyGene Expression RegulationCelastrolbiology.proteinCancer researchPentacyclic Triterpenes030217 neurology & neurosurgeryResearch PaperBritish Journal of Pharmacology
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Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models

2019

Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSA LR ) models and patient-derived myoblasts. Extra Muscleblind was functional at the molecular level and improved splicing events regulated by MBNLs in all disease models. In vivo,…

0301 basic medicinemusculoskeletal diseasesMaleRNA SplicingRNA-binding proteinBiologyMyotonic dystrophychloroquinemuscleblindMyoblasts03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAutophagyMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophytherapyMultidisciplinarymyotonic dystrophyMusclesRNANuclear ProteinsRNA-Binding ProteinsChloroquinemedicine.diseaseMyotoniaCell biologyDNA-Binding ProteinsDisease Models Animal030104 developmental biologyPhenotypechemistryPNAS PlusRNA splicingDrosophilaFemaleTrinucleotide repeat expansion030217 neurology & neurosurgery
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Enzyme replacement therapy with recombinant pro-CTSD (cathepsin D) corrects defective proteolysis and autophagy in neuronal ceroid lipofuscinosis

2019

CTSD (cathepsin D) is one of the major lysosomal proteases indispensable for the maintenance of cellular proteostasis by turning over substrates of endocytosis, phagocytosis and autophagy. Consequently, CTSD deficiency leads to a strong impairment of the lysosomal-autophagy machinery. In mice and humans CTSD dysfunction underlies the congenital variant (CLN10) of neuronal ceroid lipofuscinosis (NCL). NCLs are distinct lysosomal storage disorders (LSDs) sharing various hallmarks, namely accumulation of protein aggregates and ceroid lipofuscin leading to neurodegeneration and blindness. The most established and clinically approved approach to treat LSDs is enzyme replacement therapy (ERT) aim…

0301 basic medicineproteolysisCathepsin DCathepsin DCathepsin BstorageCathepsin L03 medical and health sciencesSequestosome 1Neuronal Ceroid-LipofuscinosesAutophagymedicineAnimalsHumansEnzyme Replacement TherapyeducationMolecular BiologyMice Knockouttherapyeducation.field_of_studyTripeptidyl-Peptidase 1030102 biochemistry & molecular biologybiologyAutophagy; cathepsin D; enzyme replacement therapy; lysosome; neuronal ceroid lipofuscinosis; proteolysis; storage; therapyBrainCell BiologyFibroblastsTripeptidyl peptidase Imedicine.diseaseLRP1Cell biologyDisease Models Animal030104 developmental biologylysosomebiology.proteinAllograft inflammatory factor 1Neuronal ceroid lipofuscinosisneuronal ceroid lipofuscinosisLysosomesResearch PaperAutophagy
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Imaging Noncanonical Autophagy and LC3-Associated Phagocytosis in Cultured Cells

2019

International audience; Monitoring of ATG8 proteins by western blotting and immunofluorescence microscopy are the most common methods to monitor the autophagy pathway. However, it has recently been shown that ATG8 proteins can be lipidated to non-autophagosome, single-membrane compartments through a noncanonical autophagy pathway. This is commonly found to occur during macro-endocytic processes such as phagocytosis, where it has been termed LC3-associated phagocytosis, and upon lysosomotropic drug treatment. Therefore, care is required when interpreting data based on ATG8 in order to conclude whether a signal relates to the canonical or noncanonical pathway. Here we provide methods to monit…

0303 health sciencesChemistryATG8PhagocytosisAutophagyImmunofluorescence MicroscopyATG8 Proteins3. Good healthCell biologyBlot03 medical and health sciencesDrug treatment0302 clinical medicinePhagocytosisLAPFluorescence microscopeLC3Noncanonical autophagy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyATG8030217 neurology & neurosurgery030304 developmental biology
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Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans

2017

AbstractAutophagy is a ubiquitous catabolic process, which causes cellular bulk degradation of cytoplasmic components and thereby regulates cellular homeostasis. Inactivation of autophagy has been linked with detrimental effects to cells and organisms. The antagonistic pleiotropy theory postulates that fitness promoting genes during youth are harmful during aging (Williams 1957). On this basis we examined genes mediating post-reproductive longevity using an RNA interference screen. From this screen we identified 30 novel regulators of post-reproductive longevity including pha-4. Through downstream analysis of pha-4 we identify that genes governing the early stages of autophagy up until the …

0303 health sciencesmedia_common.quotation_subjectNeurodegenerationAutophagyLongevityCellular homeostasisContext (language use)Biologymedicine.diseaseCell biology03 medical and health sciences0302 clinical medicineRNA interferencePleiotropymedicineGene030217 neurology & neurosurgery030304 developmental biologymedia_common
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Molecular mechanisms of endomembrane trafficking in plants

2021

Abstract Endomembrane trafficking is essential for all eukaryotic cells. The best-characterized membrane trafficking organelles include the endoplasmic reticulum (ER), Golgi apparatus, early and recycling endosomes, multivesicular body, or late endosome, lysosome/vacuole, and plasma membrane. Although historically plants have given rise to cell biology, our understanding of membrane trafficking has mainly been shaped by the much more studied mammalian and yeast models. Whereas organelles and major protein families that regulate endomembrane trafficking are largely conserved across all eukaryotes, exciting variations are emerging from advances in plant cell biology research. In this review, …

AcademicSubjects/SCI01280EndosomeENDOPLASMIC-RETICULUMGolgi ApparatusPlant ScienceSUSPENSION-CULTURED CELLSBiologyDOMAIN-CONTAINING PROTEINSEndoplasmic ReticulumEndocytosissymbols.namesakeLysosomeAutophagymedicineEndomembrane systemVACUOLAR TRAFFICKINGPlant Physiological PhenomenaLate endosomeAcademicSubjects/SCI01270AcademicSubjects/SCI02288AcademicSubjects/SCI02287Endoplasmic reticulumAcademicSubjects/SCI02286AutophagyBiology and Life SciencesBiological TransportRETICULUM EXPORT SITESCell BiologyGolgi apparatusCLATHRIN-MEDIATED ENDOCYTOSISEndocytosisFocus on Cell BiologyCell biologyTRANS-GOLGI NETWORKEditorialmedicine.anatomical_structureP24 FAMILY PROTEINSMEMBRANE TRAFFICKINGPLASMA-MEMBRANEVacuolessymbolsThe Plant Cell
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CD4 T lymphocyte autophagy is upregulated in the salivary glands of primary Sjögren’s syndrome patients and correlates with focus score and disease a…

2017

Background Primary Sjögren’s syndrome (pSS) is a common chronic autoimmune disease characterized by lymphocytic infiltration of exocrine glands and peripheral lymphocyte perturbation. In the current study, we aimed to investigate the possible pathogenic implication of autophagy in T lymphocytes in patients with pSS. Methods Thirty consecutive pSS patients were recruited together with 20 patients affected by sicca syndrome and/or chronic sialoadenitis and 30 healthy controls. Disease activity and damage were evaluated according to SS disease activity index, EULAR SS disease activity index, and SS disease damage index. T lymphocytes were analyzed for the expression of autophagy-specific marke…

AdultCD4-Positive T-LymphocytesMale0301 basic medicinePathologymedicine.medical_specialtylcsh:Diseases of the musculoskeletal systemAutophagy; Cytokines; Lymphocytes; Sjögren syndrome; Immunology and Allergy; Rheumatology; ImmunologyLymphocyteImmunologySjögren syndromeSalivary GlandsPathogenesis03 medical and health sciencesImmune systemRheumatologystomatognathic systemSicca syndromeAutophagymedicineImmunology and AllergyHumansLymphocytesCytokineAgedSjögren syndrome; Autophagy; Lymphocytes; CytokinesAutoimmune diseaseSalivary glandbusiness.industryAutophagyT lymphocyteMiddle Agedmedicine.diseaseSjögren syndromeUp-RegulationSettore MED/16 - Reumatologiastomatognathic diseasesSjogren's Syndrome030104 developmental biologymedicine.anatomical_structureImmunologyCytokinesLymphocyteFemalelcsh:RC925-935businessResearch ArticleArthritis Research & Therapy
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Hypoxic macrophages impair autophagy in epithelial cells through Wnt1: relevance in IBD.

2014

A defective induction of epithelial autophagy may have a role in the pathogenesis of inflammatory bowel diseases. This process is regulated mainly by extracellular factors such as nutrients and growth factors and is highly induced by diverse situations of stress. We hypothesized that epithelial autophagy is regulated by the immune response that in turn is modulated by local hypoxia and inflammatory signals present in the inflamed mucosa. Our results reveal that HIF-1 alpha and Wnt1 were co-localized with CD68 in cells of the mucosa of IBD patients. We have observed increased protein levels of beta-catenin, phosphorylated mTOR, and p62 and decreased expression of LC3II in colonic epithelial …

AdultMaleAdolescentImmunologyWnt1 ProteinBiologyYoung AdultImmune systemAutophagyExtracellularHumansImmunology and AllergyIntestinal MucosaWNT1Wnt Signaling PathwayPI3K/AKT/mTOR pathwayRegulation of gene expressionCD68MacrophagesTOR Serine-Threonine KinasesAutophagyWnt signaling pathwayEpithelial CellsMiddle AgedHypoxia-Inducible Factor 1 alpha SubunitInflammatory Bowel DiseasesCell HypoxiaCell biologyGene Expression RegulationFemale
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Replication of interleukin 23 receptor and autophagy-related 16-like 1 association in adult- and pediatric-onset inflammatory bowel disease in Italy.

2008

AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD genes. METHODS: Total of 763 patients with Crohn's disease (CD, 189 diagnosed at age < 19 years), 843 with ulcerative colitis (UC, 179 diagnosed < 19 years), 749 healthy controls, and 546 healthy parents (273 trios) were included in the study. The rs2241880 [autophagy-related 16-like 1 (ATG16L1)], rs11209026 and rs7517847 [interleukin 23 receptor (IL23R)], rs2066844, rs2066845, rs2066847 (CARD15), rs1050152 (OCTN1), and rs2631367 (OCTN2) gene variants were genotyped. RESULTS: The f…

AdultMaleInterleukin-23 receptorAdolescentGenotypeOrganic Cation Transport ProteinsIBDNod2 Signaling Adaptor ProteinAutophagy-Related Proteinsdigestive systemPolymorphism Single NucleotideInflammatory bowel diseaseYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaCrohn DiseaseIL23RClinical ResearchmedicineGenetic predispositionHumansGenetic Predisposition to DiseaseAge of OnsetYoung adultChildSolute Carrier Family 22 Member 5ReceptorAgedCrohn's diseaseSymportersbusiness.industryGastroenterologyInfantReceptors InterleukinGeneral MedicineMiddle AgedInflammatory Bowel Diseasesmedicine.diseaseUlcerative colitisdigestive system diseasesLogistic ModelsItalyCase-Control StudiesChild PreschoolImmunologyFemaleAge of onsetCarrier Proteinsbusiness
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Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis …

2013

OBJECTIVES: Interleukin (IL)-23 has been implicated in the pathogenesis of ankylosing spondylitis (AS). The aim of the study was to clarify the mechanisms underlying the increased IL-23 expression in the gut of AS patients. METHODS: Consecutive gut biopsies from 30 HLA-B27(+) AS patients, 15 Crohn's disease (CD) patients and 10 normal subjects were obtained. Evidence for HLA-B27 misfolding was studied. Unfolded protein response (UPR) and autophagy were assessed by RT-PCR and immunohistochemistry. The contribution of UPR and autophagy in the regulation of IL-23 expression was evaluated in in vitro experiments on isolated lamina propria mononuclear cells (LPMCs). RESULTS: Intracellular coloca…

AdultMaleProtein FoldingBiopsyImmunologyATG5Gene ExpressionInflammationdigestive systemArticleGeneral Biochemistry Genetics and Molecular BiologyATG12Young AdultCrohn DiseaseRheumatologyDownregulation and upregulationSettore BIO/13 - Biologia Applicataankylosing spondylitisAutophagymedicineInterleukin 23HumansImmunology and AllergySpondylitis AnkylosingHLA-B27 AntigenAgedMucous Membranebusiness.industryAutophagyInterleukinIleitisMiddle AgedIntestinesInterleukin 23Settore MED/16 - ReumatologiaImmunologyInterleukin-23 Subunit p19Unfolded Protein ResponseUnfolded protein responseFemalemedicine.symptombusinessAnnals of the Rheumatic Diseases
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