2023
ALKBH5 modulates hematopoietic stem and progenitor cell energy metabolism through m6A modification-mediated RNA stability control
Gao Y, Zimmer J, Vasic R, Liu C, Gbyli R, Zheng S, Patel A, Liu W, Qi Z, Li Y, Nelakanti R, Song Y, Biancon G, Xiao A, Slavoff S, Kibbey R, Flavell R, Simon M, Tebaldi T, Li H, Halene S. ALKBH5 modulates hematopoietic stem and progenitor cell energy metabolism through m6A modification-mediated RNA stability control. Cell Reports 2023, 42: 113163. PMID: 37742191, PMCID: PMC10636609, DOI: 10.1016/j.celrep.2023.113163.Peer-Reviewed Original ResearchConceptsAlkB homolog 5Post-transcriptional regulatory mechanismsHematopoietic stemNumerous cellular processesProgenitor cell fitnessEnergy metabolismMitochondrial ATP productionMethyladenosine (m<sup>6</sup>A) RNA modificationTricarboxylic acid cycleCell energy metabolismHuman hematopoietic cellsMitochondrial energy productionCell fitnessCellular processesRNA modificationsRNA methylationRegulatory mechanismsEnzyme transcriptsATP productionHomolog 5Acid cycleΑ-ketoglutarateHematopoietic cellsMessenger RNAΑ-KGAlpha-1 Adrenergic Antagonists Sensitize Neuroblastoma to Therapeutic Differentiation.
Broso F, Gatto P, Sidarovich V, Ambrosini C, De Sanctis V, Bertorelli R, Zaccheroni E, Ricci B, Destefanis E, Longhi S, Sebastiani E, Tebaldi T, Adami V, Quattrone A. Alpha-1 Adrenergic Antagonists Sensitize Neuroblastoma to Therapeutic Differentiation. Cancer Research 2023, 83: 2733-2749. PMID: 37289021, DOI: 10.1158/0008-5472.can-22-1913.Peer-Reviewed Original ResearchConceptsResidual diseaseAdrenergic antagonistsAdrenergic receptorsAlpha-1 adrenergic antagonistAdministration of doxazosinPost-consolidation therapyOverall survival probabilityPrevention of relapseHigh-risk casesMultimodal therapeutic approachPost-consolidation phaseDifferentiation of neuroblastomaNB cell viabilityAggressive childhood tumorRetinoids isotretinoinPediatric patientsΑ1B-adrenergic receptorPrevent relapseChildhood tumorsTherapeutic approachesSpecific blockadeNB cellsPharmacologic targetNeuroblastomaTumor growth
2022
Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor
Negro S, Lauria F, Stazi M, Tebaldi T, D’Este G, Pirazzini M, Megighian A, Lessi F, Mazzanti C, Sales G, Romualdi C, Fillo S, Lista F, Sleigh J, Tosolini A, Schiavo G, Viero G, Rigoni M. Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor. Acta Neuropathologica Communications 2022, 10: 189. PMID: 36567321, PMCID: PMC9791753, DOI: 10.1186/s40478-022-01495-5.Peer-Reviewed Original ResearchConceptsConnective tissue growth factorPerisynaptic Schwann cellsMotor axon terminalsTissue growth factorPro-regenerative factorsGrowth factorInjured sciatic nervePeripheral nerve injuryMotor nerve repairMonth old miceECM remodeling processDegeneration/regenerationNerve injuryCTGF levelsSciatic nerveNeuromuscular functionAxon terminalsNerve repairSchwann cellsNerve regenerationPro-regenerative signalsAxonal growthSC migrationMuscle fibersRemodeling processRecruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis
Öz H, Cheng E, Di Pietro C, Tebaldi T, Biancon G, Zeiss C, Zhang P, Huang P, Esquibies S, Britto C, Schupp J, Murray T, Halene S, Krause D, Egan M, Bruscia E. Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis. Cell Reports 2022, 41: 111797. PMID: 36516754, PMCID: PMC9833830, DOI: 10.1016/j.celrep.2022.111797.Peer-Reviewed Original ResearchConceptsC motif chemokine receptor 2Monocytes/macrophagesLung tissue damageCystic fibrosisTissue damageCF lungPulmonary neutrophilic inflammationPro-inflammatory environmentChemokine receptor 2CF lung diseaseNumber of monocytesSpecific therapeutic agentsGrowth factor βCF transmembrane conductance regulatorLung hyperinflammationLung neutrophiliaNeutrophilic inflammationNeutrophil inflammationInflammation contributesLung damageNeutrophil recruitmentLung diseaseLung tissueReceptor 2Therapeutic target