Search results for "Caspase 1"

showing 10 items of 21 documents

Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis.

2019

Background & Aims Increased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown. Methods We used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154…

0301 basic medicineLiver CirrhosisInflammasomesInterleukin-1betaArticle03 medical and health sciencesLiver diseaseMice0302 clinical medicineMice Inbred NODNon-alcoholic Fatty Liver DiseaseNLR Family Pyrin Domain-Containing 3 ProteinmedicineHepatic Stellate CellsPyroptosisAnimalsHumansLiver injuryHepatologyChemistryFatty liverCaspase 1PyroptosisInflammasomemedicine.disease3. Good healthCell biology030104 developmental biologymedicine.anatomical_structureHepatocyteHepatic stellate cellHepatocytesProtein Translocation Systems030211 gastroenterology & hepatologySteatohepatitisReactive Oxygen Speciesmedicine.drugJournal of hepatology
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Inflammasome activation in Ankylosing Spondylitis is associated to gut dysbiosis

2021

Objective: We undertook this study to evaluate the activation and functional relevance of inflammasome pathways in ankylosing spondylitis (AS) patients and rodent models and their relationship to dysbiosis. Methods: An inflammasome pathway was evaluated in the gut and peripheral blood from 40 AS patients using quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), flow cytometry, and confocal microscopy, and was compared to that of 20 healthy controls and 10 patients with Crohn’s disease. Bacteria was visualized using silver stain in human samples, and antibiotics were administered to HLA–B27–transgenic rats. The NLRP3 inhibitor MCC950 was admini…

0301 basic medicineMaleInflammasomesmedicine.medical_treatmentInterleukin-1betaInterleukin-23Mice0302 clinical medicineCrohn DiseaseNLRC4Interleukin 23Immunology and AllergyIleitisHLA-B27 AntigenSulfonamidesReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-17Interleukin-18InflammasomeIleitisMiddle AgedImmunohistochemistryAnti-Bacterial AgentsDNA-Binding ProteinsCytokineIndenesFemaleInterleukin 17Rats Transgenicmedicine.drugAdultAdolescentImmunologyReceptors Cell Surface03 medical and health sciencesAIM2Young AdultRheumatologyIleumNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumansSpondylitis AnkylosingFurans030203 arthritis & rheumatologybusiness.industryCalcium-Binding Proteinsmedicine.diseaseGastrointestinal MicrobiomeRatsCARD Signaling Adaptor Proteins030104 developmental biologyCase-Control StudiesImmunologyDysbiosisJointsbusinessDysbiosis
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Haplotypes of the caspase-1 gene, plasma caspase-1 levels, and cardiovascular risk.

2006

Caspase-1 processes the interleukin (IL)-1β and IL-18 inactive precursors to the biologically active cytokines that are known to have proatherogenic effects. The present study investigated the genetic variability of the CASP1 gene and plasma levels of caspase-1 in relation to cardiovascular risk. In Europeans, 3 tag SNPs captured 4 common haplotypes of the CASP1 gene. Among these, the A in6 allele of the G+7/in6A polymorphism was less frequent in 246 cases with myocardial infarction and a parental history of disease than in 253 controls free of familial history of disease (0.13±0.02 versus 0.20±0.02; P =0.005). However, in a larger case/control study (n=1774), these effects are borderline …

AdultMale/dk/atira/pure/subjectarea/asjc/1300/1314medicine.medical_specialtyPathologyGenotypePhysiologyPopulationMyocardial Infarction/dk/atira/pure/subjectarea/asjc/2700/2705Single-nucleotide polymorphismCoronary Artery DiseaseBiologyPolymorphism Single NucleotideRisk AssessmentCoronary artery diseaseCohort StudiesGene FrequencyPolymorphism (computer science)Internal medicinemedicineHumansGenetic Predisposition to DiseaseProspective StudiesAlleleeducationProspective cohort studyAgededucation.field_of_studyVascular diseaseHazard ratioCaspase 1Interleukin-18Genetic VariationMiddle Agedmedicine.diseaseEndocrinologyHaplotypesCardiovascular DiseasesCase-Control StudiesFemaleCardiology and Cardiovascular MedicineFollow-Up StudiesCirculation research
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Apoptosis-related Proteins in Skeletal Muscle Fibers of Spinal Muscular Atrophy

1997

There is evidence that apoptosis in spinal muscular atrophies (SMA) is not restricted to motor neurons but also affects muscle fibers. Studying the expression of several apoptosis-associated proteins we found constant expression of bax in muscle fibers, which promoted cell death. The expression of bax correlated with defective innervation of muscle fibers was also indicated by upregulation of N-CAM. While in early-onset SMA atrophic as well as normo- and hypertrophic muscle fibers displayed expression of bax, muscle fibers in late-onset SMA and peripheral neuropathies showed bax-expression only in atrophic fibers. Other investigated apoptosis-associated factors comprised interleukin-1 beta …

AdultMaleProgrammed cell deathPathologymedicine.medical_specialtyMuscle Fibers Skeletalbcl-X ProteinMuscle ProteinsApoptosisBiologyMicrofilamentPathology and Forensic MedicineMuscular Atrophy SpinalCellular and Molecular NeuroscienceReference ValuesProto-Oncogene ProteinsmedicineHumansMyocyteMuscle SkeletalActinAgedbcl-2-Associated X ProteinCaspase 1InfantPeripheral Nervous System DiseasesGeneral MedicineSpinal muscular atrophyMiddle AgedSMA*Spinal muscular atrophiesmedicine.diseaseCell biologyCysteine EndopeptidasesProto-Oncogene Proteins c-bcl-2NeurologyFemaleNeural cell adhesion moleculeNeurology (clinical)Journal of Neuropathology and Experimental Neurology
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Possible Pathomechanisms Responsible for Injury to the Central Nervous System in the Settings of Chronic Cerebrospinal Venous Insufficiency

2012

The discovery of stenoses in the azygous and internal jugular veins, the so-called chronic cerebrospinal venous insufficiency that accompanies multiple sclerosis, has enabled the reinterpretation of knowledge about this neurologic dis- ease. Pathologic venous outflow from the central nervous system appears to lead to two main problems. Firstly, it disas- sembles the blood-brain barrier and may allow the penetration of nervous parenchyma by glutamate and leukocytes. Sec- ondly, it may result in significant hypoperfusion of the brain and spinal cord. These two overlapping pathologies are likely to trigger plaques through caspase-1-driven pyroptosis of oligodendrocytes and to evoke neurodegene…

Central Nervous SystemPathologymedicine.medical_specialtyCentral nervous systemExcitotoxicityglutamatemultiple sclerosismedicine.disease_causeAxonal injuryCentral Nervous System Diseasescaspase 1venous insufficiencymedicineHumansBrachiocephalic Veinsjugular veinsPharmacologybusiness.industryMultiple sclerosisazygous veinNeurodegenerationPyroptosisGlutamate receptorGeneral Medicineblood-brain barriermedicine.diseaseSpinal cordChronic cerebrospinal venous insufficiencymedicine.anatomical_structureSpinal CordbusinessReviews on Recent Clinical Trials
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DOP21 Role of P2X7 in intestinal fibrosis and inflammasome activation: Relevance in Crohn′s Disease

2021

Abstract Background Crohn’s disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract whose etiology is unknown. CD is associated with complications such as fibrosis or fistula, which cannot be pharmacologically reversed, requiring repeated surgery. Although a profibrotic effect of the P2X7 receptor has been described in some scenarios such as lung, heart and liver, its role in intestinal fibrosis has not been analysed yet. Given the crosstalk between fibrosis and inflammasome, we aim to analyze the relevance of P2X7 in intestinal fibrosis and inflammasome activation. Methods Surgical intestinal resections of CD patients and healthy ileum of carcinoma patients were obtai…

Crohn's diseasebusiness.industryGastroenterologyCaspase 1InflammasomeGeneral Medicinemedicine.diseaseInflammatory bowel diseaseFibrosisImmunologymedicineInterleukin 18ColitisbusinessIrritable bowel syndromemedicine.drugJournal of Crohn's and Colitis
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Modeling caspase-1 inhibition: Implications for catalytic mechanism and drug design.

2019

Abstract The metabolic product of caspase-1, IL-1β, is an important mediator in inflammation and pyroptosis cell death process. Alzheimer's disease, septic shock and rheumatoid arthritis are IL-1β mediated diseases, making the caspase-1 an interesting target of pharmacological value. Many inhibitors have been developed until now, most of them are peptidomimetic with improved potency. In the present study, all-atom molecular dynamics simulations and the MM/GBSA method were employed to reproduce and interpret the results obtained by in vitro experiments for a series of inhibitors. The analysis shows that the tautomeric state of the catalytic His237 impact significantly the performance of the …

DrugModels MolecularPeptidomimeticmedia_common.quotation_subjectCaspase 1InflammationLigands01 natural sciences03 medical and health sciencesStructure-Activity RelationshipViral ProteinsMediatorDrug DiscoverymedicinePotencyHumansSerpins030304 developmental biologymedia_commonPharmacology0303 health sciencesDose-Response Relationship DrugMolecular Structure010405 organic chemistryChemistryMechanism (biology)Organic ChemistryCaspase 1PyroptosisGeneral Medicine0104 chemical sciencesBiochemistryDrug DesignBiocatalysisThermodynamicsmedicine.symptomEuropean journal of medicinal chemistry
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Induction of pyroptosis in colon cancer cells by LXRβ.

2014

Liver X receptors (LXRs) have been proposed to have some anticancer properties. We recently identified a new non-genomic role of LXRβ in colon cancer cells. Under LXR agonist treatment, LXRβ induces pyroptosis of these cells in vitro and in vivo, raising the possibility of targeting this isoform in cancer treatment.

Gene isoformAgonistCancer ResearchChemistryColorectal cancermedicine.drug_classpyroptosisCaspase 1PyroptosisNLRP3 pannexin 1medicine.diseaseIn vitro3. Good healthCell biologycolon cancerIn vivoCaspase-1medicineMolecular MedicineLXRLiver X receptorAuthor's ViewMolecularcellular oncology
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Cigarette smoke promotes inflammasome‐independent activation of caspase‐1 and ‐4 leading to gasdermin D cleavage in human macrophages

2022

Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investig…

InflammationLipopolysaccharidesPore Forming Cytotoxic Proteinsalveolar macrophages caspasecigarette smoke inflammasome lung Caspase 1 Caspases Caspases Initiator Humans Inflammation Intracellular Signaling Peptides and Proteins Lipopolysaccharides Lipopolysaccharides NLR Family Pyrin Domain-Containing 3 Protein Phosphate-Binding Proteins Pore Forming Cytotoxic Proteins Tobacco Cigarette Smoking Inflammasomes.InflammasomesSettore BIO/16 - Anatomia UmanaMacrophagesCaspase 1Intracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsBiochemistryCaspases InitiatorCigarette SmokingCaspasesNLR Family Pyrin Domain-Containing 3 ProteinTobaccoGeneticsHumansMolecular BiologyBiotechnologyThe FASEB Journal
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Potassium regulates IL-1 beta processing via calcium-independent phospholipase A2.

2000

Abstract We report that potassium leakage from cells leads to activation of the Ca2+-independent phospholipase A2 (iPLA2), and the latter plays a pivotal role in regulating the cleavage of pro-IL-1β by the IL-converting enzyme caspase-1 in human monocytes. K+ efflux led to increases of cellular levels of glycerophosphocholine, an unambiguous indicator of phospholipase A2 activation. Both maturation of IL-1β and formation of glycerophosphocholine were blocked by bromoenol lactone, the specific iPLA2 inhibitor. Bromoenol lactone-dependent inhibition of IL-1β processing was not due to perturbation of the export machinery for pro-IL-1β and IL-1β or to caspase-1 suppression. Conspicuously, activ…

Intracellular FluidPotassiumImmunologychemistry.chemical_elementNaphthalenesCleavage (embryo)MonocytesPhospholipases APhospholipase A2Calcium-Independent Phospholipase A2Immunology and AllergyHumansCells Culturedchemistry.chemical_classificationCalcium metabolismbiologyTumor Necrosis Factor-alphaCaspase 1Biological TransportCaspase InhibitorsCell biologyEnzyme ActivationPhospholipases A2EnzymechemistryPyronesbiology.proteinPotassiumCalciumEffluxBromoenol lactoneProtein Processing Post-TranslationalImmunosuppressive AgentsInterleukin-1Journal of immunology (Baltimore, Md. : 1950)
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