0000000000162390

AUTHOR

Pietro Ghezzi

0000-0003-0911-8358

showing 12 related works from this author

Redox Proteomics of the Inflammatory Secretome Identifies a Common Set of Redoxins and Other Glutathionylated Proteins Released in Inflammation, Infl…

2015

Protein cysteines can form transient disulfides with glutathione (GSH), resulting in the production of glutathionylated proteins, and this process is regarded as a mechanism by which the redox state of the cell can regulate protein function. Most studies on redox regulation of immunity have focused on intracellular proteins. In this study we have used redox proteomics to identify those proteins released in glutathionylated form by macrophages stimulated with lipopolysaccharide (LPS) after pre-loading the cells with biotinylated GSH. Of the several proteins identified in the redox secretome, we have selected a number for validation. Proteomic analysis indicated that LPS stimulated the releas…

LipopolysaccharidesProteomicsglutaredoxins; glutathione; redox signalingBlotting Westernlcsh:MedicineDown-RegulationInflammationBiologyProteomicsmedicine.disease_causeAntioxidantsDexamethasoneCell LineMiceProfilinschemistry.chemical_compoundThioredoxinsInfluenza HumanmedicineExtracellularAnimalsHumansVimentinSulfhydryl Compoundsglutathionelcsh:Scienceredox signalingglutaredoxinsInflammationMultidisciplinarylcsh:RRProteinsPeroxiredoxinsGlutathioneCell biologyBlotOxidative StressRAW 264.7 CellschemistryQR180lcsh:QTumor necrosis factor alphamedicine.symptomPeroxiredoxinOxidation-ReductionOxidative stressResearch ArticlePLOS ONE
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Cisplatin-induced peripheral neuropathy: neuroprotection by erythropoietin without affecting tumour growth

2007

This study examined the dose-dependent efficacy of erythropoietin (EPO) for preventing and/or treating cisplatin (CDDP) induced peripheral neurotoxicity (CINP), and its influence on tumour treatment and growth. Rats received eight intraperitoneal (ip) injections of 2 mg/kg CDDP twice weekly. EPO co-administered (50 or 10 microg/kg ip, three times/week) had a dose-dependent effect, partially preventing CINP, but 0.5 microg/kg ip was not effective. The neuroprotective effect lasted at least 5 weeks after the last dose of EPO and CDDP. In addition, EPO (50 microg/kg ip three times/week) after the last injection of CDDP still induced a significant recovery of CINP. In a separate experiment in r…

medicine.medical_specialtyCancer ResearchPeripheral neuropathyNeural ConductionNeurophysiologyAntineoplastic AgentsHindlimbHematocritNeuroprotectionAntineoplastic AgentInternal medicinemedicinePathologyAnimalsRats WistarErythropoietinCisplatincisplatin; Erythropoietin; peripheral neuropathy; tumor growthmedicine.diagnostic_testDose-Response Relationship Drugbusiness.industryAnimalNeurotoxicityPeripheral Nervous System DiseasesMammary Neoplasms ExperimentalTumour growthHematologymedicine.diseaseRatsHindlimbDose–response relationshipPeripheral neuropathyEndocrinologyOncologyHematocritErythropoietinRatFemalePeripheral Nervous System DiseaseCisplatinbusinessCell Divisionmedicine.drug
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Is erythropoietin a worthy candidate for traumatic brain injury or are we heading the wrong way? [version 1; referees: 2 approved]

2016

Traumatic brain injury (TBI) is a leading cause of death and disability in the modern society. Although primary prevention is the only strategy that can counteract the primary brain damage, numerous preclinical studies have been accumulated in order to find therapeutic strategies against the secondary damage. In this scenario erythropoietin (EPO) has been shown to be a promising candidate as neuroprotective agent. A recent clinical trial, however, has shown that EPO has not an overall effect on outcomes following TBI thus renewing old concerns.  However, the results of a prespecified sensitivity analysis indicate that the effect of EPO on mortality remains still unclear. In the light of the…

Molecular PharmacologyNeuropharmacology & Psychopharmacologylcsh:Rlcsh:Medicinelcsh:Qlcsh:ScienceF1000Research
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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor {kappa}B.

2009

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-kappaB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-kappaB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-kappaB inhibits NF-kappaB-driven, M1-polariz…

in vivoinflammationp50 NF-κB macrophage polarizationin vitroM1 (classic) macrophageM2 (alternative) macrophagep50 nuclear factor KappaB
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Derivatives of Erythropoietin That Are Tissue Protective But Not Erythropoietic

2004

Erythropoietin (EPO) is both hematopoietic and tissue protective, putatively through interaction with different receptors. We generated receptor subtype–selective ligands allowing the separation of EPO's bioactivities at the cellular level and in animals. Carbamylated EPO (CEPO) or certain EPO mutants did not bind to the classical EPO receptor (EPOR) and did not show any hematopoietic activity in human cell signaling assays or upon chronic dosing in different animal species. Nevertheless, CEPO and various nonhematopoietic mutants were cytoprotective in vitro and conferred neuroprotection against stroke, spinal cord compression, diabetic neuropathy, and experimental autoimmune encephalomyeli…

Encephalomyelitis Autoimmune ExperimentalEncephalomyelitiscarbamylated erythropoietinApoptosisPharmacologyLigandsNeuroprotectionRats Sprague-DawleyMiceStructure-Activity RelationshipDiabetic Neuropathiesddc:570hemic and lymphatic diseasesReceptors ErythropoietinmedicineAnimalsHumansErythropoiesisReceptorErythropoietinCells CulturedNeuronsMice Inbred C3HBinding SitesMultidisciplinaryChemistryExperimental autoimmune encephalomyelitisErythropoietin; erythropoietin receptor; carbamylated erythropoietin; neuroprotective agentsmedicine.diseaseRecombinant ProteinsRatsErythropoietin receptorStrokeNeuroprotective AgentsErythropoietin Erythropoietin derivative NeuroprotectionHematocritMutagenesisErythropoietinDrug DesignImmunologyErythropoiesisFemaleNervous System DiseasesSignal transductionerythropoietin receptorSpinal Cord CompressionSignal Transductionmedicine.drugScience
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Response to I. Batinic-Haberle et al.

2016

Letter to the editor.-- et al.

0301 basic medicinePhysiologybusiness.industryChemistryClinical BiochemistryCell Biologycomputer.software_genreBiochemistry03 medical and health sciences030104 developmental biologyComputingMethodologies_DOCUMENTANDTEXTPROCESSINGGeneral Earth and Planetary SciencesArtificial intelligencebusinessMolecular BiologycomputerNatural language processingGeneral Environmental ScienceAntioxidants & Redox Signaling
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Erythropoietin mediates tissue protection through an erythropoietin and common beta-subunit heteroreceptor

2004

The cytokine erythropoietin (Epo) is tissue-protective in preclinical models of ischemic, traumatic, toxic, and inflammatory injuries. We have recently characterized Epo derivatives that do not bind to the Epo receptor (EpoR) yet are tissue-protective. For example, carbamylated Epo (CEpo) does not stimulate erythropoiesis, yet it prevents tissue injury in a wide variety ofin vivoandin vitromodels. These observations suggest that another receptor is responsible for the tissue-protective actions of Epo. Notably, prior investigation suggests that EpoR physically interacts with the common β receptor (βcR), the signal-transducing subunit shared by the granulocyte-macrophage colony stimulating fa…

Time FactorsBiologyMotor ActivityHeteroreceptorNeuroprotectionCell LineMicemedicineReceptors ErythropoietinAnimalsVentricular Functionerythropoietin receptor; common beta receptor; tissue injury; CytokinesReceptorErythropoietinAortaCells CulturedSpinal Cord InjuriesMice KnockoutMultidisciplinaryCell MembraneBiological SciencesErythropoietin Erythropoietin receptor neuroprotectionErythropoietin receptorCell biologyMice Inbred C57BLProtein SubunitsErythrocyte maturationErythropoietinKnockout mouseImmunologyErythropoiesismedicine.drug
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Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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Corrigendum to “European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS…

2018

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics b…

0301 basic medicineSocieties ScientificRedox signalingInternational CooperationClinical BiochemistryNanotechnologyReview ArticleBiologyPublic administrationBiochemistryAntioxidantsArticle03 medical and health sciencesmedia_common.cataloged_instanceAnimalsHumansCost actionEuropean UnionEuropean unionMolecular Biologylcsh:QH301-705.5media_commonFunding AgencyRedox therapeuticslcsh:R5-920Organic ChemistryReactive nitrogen species030104 developmental biologyWork (electrical)lcsh:Biology (General)Oxidative stressReactive Oxygen Specieslcsh:Medicine (General)Oxidation-ReductionSignal TransductionRedox Biology
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Is erythropoietin a worthy candidate for traumatic brain injury or are we heading the wrong way?

2016

Traumatic brain injury (TBI) is a leading cause of death and disability in the modern society. Although primary prevention is the only strategy that can counteract the primary brain damage, numerous preclinical studies have been accumulated in order to find therapeutic strategies against the secondary damage. In this scenario erythropoietin (EPO) has been shown to be a promising candidate as neuroprotective agent. A recent clinical trial, however, has shown that EPO has not an overall effect on outcomes following TBI thus renewing old concerns.  However, the results of a prespecified sensitivity analysis indicate that the effect of EPO on mortality remains still unclear. In the light of the…

0301 basic medicinemedicine.medical_specialtyMolecular PharmacologyNeuropharmacology & PsychopharmacologyTraumatic brain injurySolid baseBrain damageNeuroprotectionGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTraumatic brain injury0302 clinical medicinePrimary preventionmedicineGeneral Pharmacology Toxicology and PharmaceuticsIntensive care medicineErythropoietin; Neuroprotection; Traumatic brain injuryErythropoietinCause of deathGeneral Immunology and Microbiologybusiness.industryArticlesGeneral MedicineOpinion Articlemedicine.diseaseNeuroprotectionClinical trial030104 developmental biologyErythropoietinmedicine.symptombusinessNeuroscience030217 neurology & neurosurgerymedicine.drugF1000Research
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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

2009

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-kappaB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-kappaB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-kappaB inhibits NF-kappaB-driven, M1-polariz…

LipopolysaccharidesP50Macrophage polarizationRegulatorInflammationBiologyImmune toleranceMiceCell polaritymedicineImmune ToleranceMacrophageAnimalsHumansCells CulturedMice KnockoutMultidisciplinaryMacrophagesCell PolarityNF-kappa B p50 SubunitNF-kappa B p50 SubunitInterferon-betaBiological SciencesCell biologyEndotoxinsSTAT1 Transcription FactorImmunologymedicine.symptom
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European contribution to the study of ROS : A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

2017

WOS: 000410470000009

0301 basic medicinereactive oxygen species ; reactive nitrogen species ; redox signaling ; oxidative stress ; antioxidants ; redox therapeuticsRedox signalingInternational CooperationSMOOTH-MUSCLE-CELLS[SDV]Life Sciences [q-bio]Clinical BiochemistryISCHEMIA-REPERFUSION INJURYReviewddc:616.07Bioinformaticsmedicine.disease_causeBiochemistryAntioxidants0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCost actionlcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSmedia_commonlcsh:R5-920Redox therapeuticsReactive nitrogen species3. Good healthVariety (cybernetics)MANGANESE SUPEROXIDE-DISMUTASECHRONIC GRANULOMATOUS-DISEASERisk analysis (engineering)ddc:540lcsh:Medicine (General)Oxidation-ReductionSignal TransductionSocieties ScientificPULMONARY ARTERIAL-HYPERTENSIONMedicinaEstrès oxidatiuBiology03 medical and health sciencesAntioxidants ; Oxidative Stress ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Redox Signaling ; Redox TherapeuticsJournal Articlemedicinemedia_common.cataloged_instanceAnimalsHumans[CHIM]Chemical SciencesEuropean UnionEuropean unionNITRIC-OXIDE SYNTHASETANDEM MASS-SPECTROMETRYMolecular BiologyMITOCHONDRIAL OXIDATIVE STRESSGROWTH-FACTOR-BETAOrganic ChemistryDisease progressionBiology and Life SciencesOxidation reductionManganese Superoxide Dismutase030104 developmental biologylcsh:Biology (General)Oxidative stressReactive oxygen species030217 neurology & neurosurgeryOxidative stressRedox biology
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