Michael Rehman, PhD
Associate Research ScientistCards
About
Research
Publications
2021
Wet-dry-wet drug screen leads to the synthesis of TS1, a novel compound reversing lung fibrosis through inhibition of myofibroblast differentiation
Ring NAR, Volpe MC, Stepišnik T, Mamolo MG, Panov P, Kocev D, Vodret S, Fortuna S, Calabretti A, Rehman M, Colliva A, Marchesan P, Camparini L, Marcuzzo T, Bussani R, Scarabellotto S, Confalonieri M, Pham TX, Ligresti G, Caporarello N, Loffredo FS, Zampieri D, Džeroski S, Zacchigna S. Wet-dry-wet drug screen leads to the synthesis of TS1, a novel compound reversing lung fibrosis through inhibition of myofibroblast differentiation. Cell Death & Disease 2021, 13: 2. PMID: 34916483, PMCID: PMC8677786, DOI: 10.1038/s41419-021-04439-4.Peer-Reviewed Original ResearchConceptsAnti-fibrotic effectsDopamine receptor 3Lung fibrosisMyofibroblast activationReceptor 3Idiopathic pulmonary fibrosis patientsMyofibroblast differentiationPulmonary fibrosis patientsProgression of fibrosisTransforming Growth Factor-β PathwayGrowth factor β pathwayHigh-throughput screenDisease progressionMurine modelFibrosisFibrosis patientsFibrotic diseasesDrug screensLung fibroblastsNovel compoundsProgressionΒ pathwayImportant targetDopaminePrimary fibroblastsA ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis
Pradella D, Deflorian G, Pezzotta A, Di Matteo A, Belloni E, Campolungo D, Paradisi A, Bugatti M, Vermi W, Campioni M, Chiapparino A, Scietti L, Forneris F, Giampietro C, Volf N, Rehman M, Zacchigna S, Paronetto MP, Pistocchi A, Eichmann A, Mehlen P, Ghigna C. A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis. Nature Communications 2021, 12: 4872. PMID: 34381052, PMCID: PMC8358048, DOI: 10.1038/s41467-021-24998-6.Peer-Reviewed Original ResearchConceptsSplicing isoformsNetrin-1 bindingAlternative splicing factorPost-transcriptional pathwayNetrin-1 receptor UNC5BBlood vessel developmentEndothelial cellsApoptosis-dependent mannerSplicing factorsApoptotic functionTumor angiogenesisNetrin-1Vascular developmentVessel developmentInduces ApoptosisReceptor UNC5BIsoformsApoptosisUNC5BAngiogenesisExonsRegulatorPoor patient outcomesCancer vasculaturePathwayA Polyphenol-Rich Extract of Olive Mill Wastewater Enhances Cancer Chemotherapy Effects, While Mitigating Cardiac Toxicity
Albini A, Festa M, Ring N, Baci D, Rehman M, Finzi G, Sessa F, Zacchigna S, Bruno A, Noonan D. A Polyphenol-Rich Extract of Olive Mill Wastewater Enhances Cancer Chemotherapy Effects, While Mitigating Cardiac Toxicity. Frontiers In Pharmacology 2021, 12: 694762. PMID: 34434106, PMCID: PMC8381749, DOI: 10.3389/fphar.2021.694762.Peer-Reviewed Original ResearchHearts of miceSide effectsRat cardiomyocytesPotential cardioprotective activityEffect of chemotherapyProstate cancer xenograftsAdverse side effectsColon cancer cell growthCancer cell growthPolyphenol-rich extractAnti-oxidant activityAnti-cancer activityCardiovascular preventionCardioprotective effectsTumor weightCardiac toxicityCancer patientsCardiovascular toxicityCancer xenograftsCardioprotective roleProtective effectCancer chemotherapy effectsMouse pupsCardioprotective activityChemotherapy effectA Polyphenol-Rich Extract of Olive Mill Wastewater Enhances Cancer Chemotherapy Effects, While Mitigating Cardiac Toxicity
Albini Adriana, Festa Marco M. G., Ring Nadja, Baci Denisa, Rehman Michael, Finzi Giovanna, Sessa Fausto, Zacchigna Serena, Bruno Antonino, Noonan Douglas M.Peer-Reviewed Original Research
2020
Genetic lineage tracing reveals poor angiogenic potential of cardiac endothelial cells
Kocijan T, Rehman M, Colliva A, Groppa E, Leban M, Vodret S, Volf N, Zucca G, Cappelletto A, Piperno GM, Zentilin L, Giacca M, Benvenuti F, Zhou B, Adams R, Zacchigna S. Genetic lineage tracing reveals poor angiogenic potential of cardiac endothelial cells. Cardiovascular Research 2020, 117: 256-270. PMID: 31999325, PMCID: PMC7797216, DOI: 10.1093/cvr/cvaa012.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsApelinCalcium-Binding ProteinsCell Line, TumorCell LineageCell ProliferationCellular MicroenvironmentCoronary VesselsEndothelial CellsMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicMuscle, SkeletalNeoplasmsNeovascularization, PathologicNeovascularization, PhysiologicPhenotypeReceptor, Notch1Tumor BurdenTumor MicroenvironmentVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1ConceptsGenetic lineage tracingCardiac endothelial cellsPro-angiogenic stimuliEndothelial cellsAngiogenic responseSkeletal muscleCardiac ischaemiaApelin expressionLineage tracingAngiogenic potentialCancer cellsVascular endothelial growth factorMyocardial infarction resultsReduced tumor angiogenesisEndothelial growth factorPro-angiogenic moleculesSurgical revascularizationInfarction resultsClinical trialsContractile functionNew arteriolesSame doseTumor massTherapeutic revascularizationCardiomyocyte death
2019
Rhomboid-Like-2 Intramembrane Protease Mediates Metalloprotease-Independent Regulation of Cadherins
Battistini C, Rehman M, Avolio M, Arduin A, Valdembri D, Serini G, Tamagnone L. Rhomboid-Like-2 Intramembrane Protease Mediates Metalloprotease-Independent Regulation of Cadherins. International Journal Of Molecular Sciences 2019, 20: 5958. PMID: 31783481, PMCID: PMC6928865, DOI: 10.3390/ijms20235958.Peer-Reviewed Original ResearchConceptsE-cadherin extracellular domainIntramembrane proteasesExtracellular domainPost-translational regulationSame functional pathwayRhomboid familyRHBDL2Tissue homeostasisNovel regulatorCell motilityNegative regulatorFunctional pathwaysCadherinMajor familiesCell migrationAdhesive receptorsFunctional roleNovel mechanismVE-cadherinNovel MMPsE-cadherinCancer cellsRegulatorProteaseEndothelial cellsmiR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation
Moimas S, Salton F, Kosmider B, Ring N, Volpe MC, Bahmed K, Braga L, Rehman M, Vodret S, Graziani ML, Wolfson MR, Marchetti N, Rogers TJ, Giacca M, Criner GJ, Zacchigna S, Confalonieri M. miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation. ERJ Open Research 2019, 5: 00138-2019. PMID: 31857992, PMCID: PMC6911923, DOI: 10.1183/23120541.00138-2019.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisMiR-200 family membersEpithelial-mesenchymal transitionATII cellsEMT markersATI cellsMarker expressionFamily membersRegenerative potentialAlveolar type II cellsType II cellsIPF patientsSenescence marker expressionIPF lungsMiR-200 familyPulmonary fibrosisEpithelial cell transdifferentiationCell markersImpaired expressionFamilial casesCell transdifferentiationII cellsSenescent phenotypeMicroRNA effectsTransdifferentiationLoss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression
Eiber N, Rehman M, Kravic B, Rudolf R, Sandri M, Hashemolhosseini S. Loss of Protein Kinase Csnk2b/CK2β at Neuromuscular Junctions Affects Morphology and Dynamics of Aggregated Nicotinic Acetylcholine Receptors, Neuromuscular Transmission, and Synaptic Gene Expression. Cells 2019, 8: 940. PMID: 31434353, PMCID: PMC6721821, DOI: 10.3390/cells8080940.Peer-Reviewed Original ResearchConceptsSynaptic gene expressionGene expressionNicotinic acetylcholine receptorsClustering of AChRsNeuromuscular junctionCultured muscle cellsAcetylcholine receptorsDistinctive proteinsCK2Neuromuscular transmissionAChR clustersΒ-subunitCompound muscle action potentialHigh turnover rateCK2βCell proliferationMuscle action potentialsNMJ fragmentationSkeletal muscle fibersPrecise roleAge-dependent decreaseMuscle cellsAcetylcholine esterase inhibitorsAChRExpressionHigh-throughput screening discovers antifibrotic properties of haloperidol by hindering myofibroblast activation
Rehman M, Vodret S, Braga L, Guarnaccia C, Celsi F, Rossetti G, Martinelli V, Battini T, Long C, Vukusic K, Kocijan T, Collesi C, Ring N, Skoko N, Giacca M, Del Sal G, Confalonieri M, Raspa M, Marcello A, Myers MP, Crovella S, Carloni P, Zacchigna S. High-throughput screening discovers antifibrotic properties of haloperidol by hindering myofibroblast activation. JCI Insight 2019, 4: e123987. PMID: 30996132, PMCID: PMC6538355, DOI: 10.1172/jci.insight.123987.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCalciumCell DifferentiationCells, CulturedDisease Models, AnimalDrug RepositioningEndoplasmic Reticulum StressFibrosisHaloperidolHumansIntravital MicroscopyLungMiceMyocardiumMyofibroblastsOptical ImagingPrimary Cell CultureReceptor, Notch1Receptors, sigmaRNA InterferenceRNA, Small InterferingSignal TransductionConceptsMyofibroblast activationSigma receptor 1Smooth muscle actinDifferent animal modelsTransforming Growth FactorDiscovery of haloperidolTumor-associated fibrosisMechanism of actionEndoplasmic reticulum stress responseFibrotic burdenAntifibrotic effectsAntifibrotic propertiesCommon antipsychotic drugsAntipsychotic drugsFibrotic processIntracellular calciumReticulum stress responseAnimal modelsMuscle actinFibrotic conditionsHaloperidolReceptor 1Growth factorContractile proteinsTherapeutic solutions
2018
Paracrine effect of regulatory T cells promotes cardiomyocyte proliferation during pregnancy and after myocardial infarction
Zacchigna S, Martinelli V, Moimas S, Colliva A, Anzini M, Nordio A, Costa A, Rehman M, Vodret S, Pierro C, Colussi G, Zentilin L, Gutierrez MI, Dirkx E, Long C, Sinagra G, Klatzmann D, Giacca M. Paracrine effect of regulatory T cells promotes cardiomyocyte proliferation during pregnancy and after myocardial infarction. Nature Communications 2018, 9: 2432. PMID: 29946151, PMCID: PMC6018668, DOI: 10.1038/s41467-018-04908-z.Peer-Reviewed Original ResearchConceptsRegulatory T cellsMyocardial infarctionTreg depletionCardiomyocyte proliferationT cellsRole of TregsDepressed cardiac functionFetal cardiomyocyte proliferationPregnancy decreasesInfarct sizeMaternal toleranceMassive inflammationPregnant mothersCardiac functionMaternal bloodTherapeutic effectParacrine mannerTregsCollagen depositionParacrine effectsPregnant animalsInfarctionProliferationCardiomyocytesProliferative cardiomyocytes