Search results for "hmgb1"

showing 10 items of 21 documents

TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
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Administration of all‐ trans retinoic acid after experimental traumatic brain injury is brain protective

2020

BACKGROUND AND PURPOSE: All‐trans retinoic acid (ATRA) is a vitamin A metabolite, important in the developing and mature brain. Pre‐injury ATRA administration ameliorates ischaemic brain insults in rodents. This study examined the effects of post‐traumatic ATRA treatment in experimental traumatic brain injury (TBI). EXPERIMENTAL APPROACH: Male adult mice were subjected to the controlled cortical impact model of TBI or sham procedure and killed at 7 or 30 days post‐injury (dpi). ATRA (10 mg kg−1, i.p.) was given immediately after the injury and 1, 2 and 3 dpi. Neurological function and sensorimotor coordination were evaluated. Brains were processed for (immuno‐) histological, mRNA and protei…

Male0301 basic medicineTraumatic brain injuryRetinoic acidTretinoinPharmacologyHippocampal formationHMGB1Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsInflammationPharmacologyMicrogliabiologybusiness.industryBrainmedicine.diseaseGranule cellResearch PapersAstrogliosis030104 developmental biologymedicine.anatomical_structurechemistryBlood-Brain BarrierApoptosisbiology.proteinbusiness030217 neurology & neurosurgeryBritish Journal of Pharmacology
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Haem oxygenase-1 down-regulates high mobility group box 1 and matrix metalloproteinases in osteoarthritic synoviocytes

2010

Objectives. Activation of osteoarthritic synoviocytes by pro-inflammatory cytokines results in the release of biochemical mediators such as MMPs and high mobility group box 1 (HMGB1). Extracellular HMGB1 can play an important role in joint diseases as a mediator of synovitis. We have shown previously that haem oxygenase-1 (HO-1) exerts protective effects during inflammatory responses. In this study, we have examined whether HO-1 induction would be an effective strategy to control MMP and HMGB1 production in osteoarthritic synoviocytes. Methods. Osteoarthritic synoviocytes were obtained by digestion with collagenase and cultured until third passage. HO-1 was induced by cobalt protoporphyrin …

MaleAnalysis of VarianceSmall interfering RNASynovial MembraneDown-RegulationTransfectionBiologyMatrix metalloproteinaseHMGB1COPPMolecular biologyMatrix MetalloproteinasesRheumatologyOsteoarthritisGene expressionbiology.proteinHumansGene silencingInterstitial collagenaseFemalePharmacology (medical)HMGB1 ProteinCells CulturedHeme Oxygenase-1AgedRheumatology
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High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes

2010

Introduction High mobility group box 1 (HMGB1) is released by necrotic cells or secreted in response to inflammatory stimuli. Extracellular HMGB1 may act as a pro-inflammatory cytokine in rheumatoid arthritis. We have recently reported that HMGB1 is released by osteoarthritic synoviocytes after activation with interleukin-1beta (IL-1β) The present study investigated the role of HMGB1 in synovial inflammation in osteoarthritis (OA). Methods HMGB1 was determined in human synovium using immunohistochemistry, comparing normal to OA. OA synoviocytes were incubated with HMGB1 at 15 or 25 ng/ml in the absence or presence of IL-1β (10 ng/ml). Gene expression was analyzed by quantitative PCR and pro…

MaleChemokineMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaImmunologyInflammationchemical and pharmacologic phenomenaCCL2HMGB1p38 Mitogen-Activated Protein KinasesRheumatologySynovitisMatrix Metalloproteinase 13HumansMedicineImmunology and AllergyRNA MessengerHMGB1 ProteinExtracellular Signal-Regulated MAP KinasesCells CulturedAgedbiologybusiness.industrySynovial MembraneNF-kappa BOsteoarthritis Kneemedicine.diseaseImmunohistochemistryMolecular biologyCCL20Cytokinemedicine.anatomical_structurebiology.proteinFemaleMatrix Metalloproteinase 3Matrix Metalloproteinase 1Synovial membranemedicine.symptombusinessProto-Oncogene Proteins c-aktResearch ArticleArthritis Research & Therapy
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Comparative Analysis of Chromatin-Delivered Biomarkers in the Monitoring of Sepsis and Septic Shock: A Pilot Study

2021

Sepsis management remains one of the most important challenges in modern clinical practice. Rapid progression from sepsis to septic shock is practically unpredictable, hence the critical need for sepsis biomarkers that can help clinicians in the management of patients to reduce the probability of a fatal outcome. Circulating nucleoproteins released during the inflammatory response to infection, including neutrophil extracellular traps, nucleosomes, and histones, and nuclear proteins like HMGB1, have been proposed as markers of disease progression since they are related to inflammation, oxidative stress, endothelial damage, and impairment of the coagulation response, among other pathological…

MalePilot Projectslaw.inventionCohort StudiesHistonessepsisMicelawHMGB1 ProteinBiology (General)SpectroscopyImmunoassayHMGB1biologyCommunicationAntibodies MonoclonalGeneral MedicineMiddle AgedIntensive care unitShock SepticChromatinComputer Science ApplicationsChemistryCohortFemaleELISAmedicine.symptomcirculating histonesmedicine.medical_specialtyQH301-705.5InflammationHMGB1CatalysisInorganic ChemistrySepsismedicineAnimalsHumansPhysical and Theoretical ChemistryIntensive care medicineMolecular BiologyPathologicalQD1-999Septic shockbusiness.industryOrganic ChemistrybiomarkersNeutrophil extracellular trapsmedicine.diseaseNucleoproteinsnucleosomesbiology.proteinCitrullineseptic shockbusinessInternational Journal of Molecular Sciences
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Human malignant mesothelioma is recapitulated in immunocompetent BALB/c mice injected with murine AB cells

2016

Malignant Mesothelioma is a highly aggressive cancer, which is difficult to diagnose and treat. Here we describe the molecular, cellular and morphological characterization of a syngeneic system consisting of murine AB1, AB12 and AB22 mesothelioma cells injected in immunocompetent BALB/c mice, which allows the study of the interplay of tumor cells with the immune system. Murine mesothelioma cells, like human ones, respond to exogenous High Mobility Group Box 1 protein, a Damage-Associated Molecular Pattern that acts as a chemoattractant for leukocytes and as a proinflammatory mediator. The tumors derived from AB cells are morphologically and histologically similar to human MM tumors, and res…

Mesothelioma0301 basic medicinePathologymedicine.medical_specialtyLung NeoplasmsAntineoplastic AgentsPemetrexedHMGB1DeoxycytidineArticleProinflammatory cytokineBALB/c03 medical and health sciences0302 clinical medicineImmune systemMalignant MesotheliomCell Line TumormedicineMesothelioma HMGB1 in vivo imagingcancerAnimalsHumansMesotheliomaHMGB1 ProteinCisplatinMice Inbred BALB CMultidisciplinarybiologybusiness.industryMesothelioma Malignantbiology.organism_classificationmedicine.diseaseSurvival AnalysisGemcitabine030104 developmental biologyPemetrexedCell culturemesothelioma030220 oncology & carcinogenesisbiology.proteinFemaleCisplatinBALB/cbusinessImmunocompetenceNeoplasm Transplantationmedicine.drug
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Cationic polyaspartamide-based nanocomplexes mediate siRNA entry and down-regulation of the pro-inflammatory mediator high mobility group box 1 in ai…

2015

Abstract High-mobility group box 1 (HMGB1) is a nonhistone protein secreted by airway epithelial cells in hyperinflammatory diseases such as asthma. In order to down-regulate HMGB1 expression in airway epithelial cells, siRNA directed against HMGB1 was delivered through nanocomplexes based on a cationic copolymer of poly(N-2-hydroxyethyl)- d,l -aspartamide (PHEA) by using H441 cells. Two copolymers were used in these experiments bearing respectively spermine side chains (PHEA-Spm) and both spermine and PEG2000 chains (PHEA-PEG-Spm). PHEA-Spm and PHEA-PEG-Spm derivatives complexed dsDNA oligonucleotides with a w/w ratio of 1 and higher as shown by a gel retardation assay. PHEA-Spm and PHEA-P…

Polyaspartamide copolymerNucleic acid-based drugDown-RegulationPharmaceutical ScienceSpermineRespiratory MucosaBiologyTransfectionAirway epithelial cellsNucleic acid-based drugsFlow cytometrychemistry.chemical_compoundCell Line TumorMaterials TestingAirway epithelial cellmedicineHumansElectrophoretic mobility shift assayMTT assayDAPIRNA Small InterferingCytotoxicityPolyhydroxyethyl MethacrylateHMGB1Airway epithelial cells; HMGB1; Nucleic acid-based drugs; PHEA; Polyaspartamide copolymers; Sirnamedicine.diagnostic_testOligonucleotideMammaglobin AfungiGene Transfer TechniquesEpithelial CellsDNAPHEAMolecular biologyNanostructuresPolyaspartamide copolymerschemistrySirnaTrypan bluePeptides
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Autophagy-Dependent Anticancer Immune Responses Induced by Chemotherapeutic Agents in Mice

2011

Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recr…

Programmed cell deathcells cancer immunogenicity calreticulin exposure hmgb1Antineoplastic AgentsBiologyimmunogenicityNOMicechemistry.chemical_compoundAdenosine TriphosphateImmune systemCell Line TumorNeoplasmsAutophagyExtracellularAnimalsHumanscancerMice Inbred BALB CMultidisciplinaryCell DeathImmunogenicityAutophagyDendritic CellsMice Inbred C57BLhmgb1chemistryCell cultureCancer researchImmunogenic cell deathcellsMitoxantroneCalreticulinAdenosine triphosphatecalreticulin exposure
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