Michael Rehman, PhD
Associate Research ScientistCards
About
Research
Publications
2024
Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease
Zhang C, Rehman M, Tian X, Pei S, Gu J, Bell T, Dong K, Tham M, Cai Y, Wei Z, Behrens F, Jetten A, Zhao H, Lek M, Somlo S. Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease. Nature Communications 2024, 15: 3698. PMID: 38693102, PMCID: PMC11063051, DOI: 10.1038/s41467-024-48025-6.Peer-Reviewed Original ResearchConceptsMouse models of autosomal dominant polycystic kidney diseaseModel of autosomal dominant polycystic kidney diseasePolycystin signalingAutosomal dominant polycystic kidney diseasePolycystin-1Polycystic kidney diseaseTreat autosomal dominant polycystic kidney diseaseGlis2Primary ciliaKidney tubule cellsSignaling pathwayMouse modelDominant polycystic kidney diseasePotential therapeutic targetTranslatomeAntisense oligonucleotidesKidney diseasePolycystinMouse kidneyFunctional effectorsCyst formationTherapeutic targetInactivationFunctional targetPharmacological targetsA synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress
Fedeles B, Bhardwaj R, Ishikawa Y, Khumsubdee S, Krappitz M, Gubina N, Volpe I, Andrade D, Westergerling P, Staudner T, Campolo J, Liu S, Dong K, Cai Y, Rehman M, Gallagher A, Ruchirawat S, Croy R, Essigmann J, Fedeles S, Somlo S. A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317344121. PMID: 38241440, PMCID: PMC10823221, DOI: 10.1073/pnas.2317344121.Peer-Reviewed Original ResearchConceptsCyst cellsAutosomal dominant polycystic kidney diseaseMouse models of autosomal dominant polycystic kidney diseasePolycystic kidney diseaseModel of autosomal dominant polycystic kidney diseaseKidney diseaseDeveloped primersMitochondrial oxidative stressPathophysiology of autosomal dominant polycystic kidney diseaseOxidative stressInduce apoptosisMitochondrial respirationCystic cellsUp-regulating aerobic glycolysisHomozygous inactivationMonogenic causeDominant polycystic kidney diseaseAerobic glycolysisRenal replacement therapyApoptosisEnd-stage kidney diseaseAnti-tumor agentsAdult mouse modelChronic kidney diseaseAlkylate DNA
2023
Inactivation of Ire1alpha Endoribonuclease Domain Slows Down ADPKD in Orthologous Mouse Models
Bhardwaj R, Volpe I, Yilmaz D, Pioppini C, Roy K, Rehman M, Cai Y, Krappitz M, Somlo S, Fedeles S. Inactivation of Ire1alpha Endoribonuclease Domain Slows Down ADPKD in Orthologous Mouse Models. Journal Of The American Society Of Nephrology 2023, 34: 19-19. DOI: 10.1681/asn.20233411s119b.Peer-Reviewed Original Research
2022
Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease
Dong K, Tham M, Cordido A, Cai Y, Pei S, Bhardwaj R, Wei Z, Rehman M, Roy K, Tian X, Somlo S. Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2022, 33: 418-418. DOI: 10.1681/asn.20223311s1418c.Peer-Reviewed Original Research
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 cells