2021
EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis
Hidalgo D, Bejder J, Pop R, Gellatly K, Hwang Y, Maxwell Scalf S, Eastman AE, Chen JJ, Zhu LJ, Heuberger JAAC, Guo S, Koury MJ, Nordsborg NB, Socolovsky M. EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis. Nature Communications 2021, 12: 7334. PMID: 34921133, PMCID: PMC8683474, DOI: 10.1038/s41467-021-27562-4.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntigens, CDBcl-X ProteinCD4 AntigensCell CycleCell DifferentiationCell NucleusCell SizeCell SurvivalCyclin-Dependent Kinase Inhibitor p27Embryo, MammalianErythroblastsErythrocytesErythropoiesisErythropoietinFemaleFetusHealthy VolunteersHumansIronLiverMaleMice, Inbred C57BLModels, BiologicalProtein Serine-Threonine KinasesReceptors, ErythropoietinReceptors, TransferrinReticulocytesSignal TransductionConceptsCell size regulationCell sizeSequential cell divisionsEpoR functionErythroblast survivalMouse erythroblastsCell divisionSize regulationHuman erythropoiesisErythropoietin receptorCell cycleEpoRHypoxic stressRed cell sizeHigh erythropoietinLarger red cellsWild-type miceCyclingErythroblastsRegulationHigher EPO levelsMiceRed cellsSurvivalErythropoiesis
2019
MLL-AF9 initiates transformation from fast-proliferating myeloid progenitors
Chen X, Burkhardt DB, Hartman AA, Hu X, Eastman AE, Sun C, Wang X, Zhong M, Krishnaswamy S, Guo S. MLL-AF9 initiates transformation from fast-proliferating myeloid progenitors. Nature Communications 2019, 10: 5767. PMID: 31852898, PMCID: PMC6920141, DOI: 10.1038/s41467-019-13666-5.Peer-Reviewed Original ResearchAnimalsCell CycleCell DifferentiationCell ProliferationCell Transformation, NeoplasticCyclin D1Disease Models, AnimalFemaleGene Expression Regulation, LeukemicGene Knock-In TechniquesHumansKaplan-Meier EstimateLeukemia, Myeloid, AcuteMaleMice, TransgenicMyeloid Progenitor CellsMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionPiperazinesPrimary Cell CulturePrognosisPyridinesTargeting Fibrotic Signaling: A Review of Current Literature and Identification of Future Therapeutic Targets to Improve Wound Healing.
Hetzler PT, Dash BC, Guo S, Hsia HC. Targeting Fibrotic Signaling: A Review of Current Literature and Identification of Future Therapeutic Targets to Improve Wound Healing. Annals Of Plastic Surgery 2019, 83: e92-e95. PMID: 31246672, PMCID: PMC6851445, DOI: 10.1097/sap.0000000000001955.Peer-Reviewed Original ResearchConceptsTherapeutic targetAberrant wound healing processAppropriate physiologic responseMorbid disease processSurvival of myofibroblastsWound healingFibrotic signaling pathwaysTranscription factor/serum response factor (MRTF/SRF) pathwayFuture therapeutic targetsSmooth muscle actinFuture translational researchCurrent literatureFibrotic signalingTherapeutic optionsFibrotic lesionsTissue injuryWound healing processDisease processPhysiologic responsesSerum response factor pathwayMuscle actinFactor pathwayExcessive responseFibrosisTranslational researchMKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation
Hu X, Liu ZZ, Chen X, Schulz VP, Kumar A, Hartman AA, Weinstein J, Johnston JF, Rodriguez EC, Eastman AE, Cheng J, Min L, Zhong M, Carroll C, Gallagher PG, Lu J, Schwartz M, King MC, Krause DS, Guo S. MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation. Nature Communications 2019, 10: 1695. PMID: 30979898, PMCID: PMC6461646, DOI: 10.1038/s41467-019-09636-6.Peer-Reviewed Original ResearchConceptsCell fate reprogrammingChromatin accessibilityActin cytoskeletonSomatic cell reprogrammingPluripotency transcription factorsGlobal chromatin accessibilityGenomic accessibilityCytoskeleton (LINC) complexCell reprogrammingCytoskeletal genesTranscription factorsReprogrammingPluripotencyChromatinCytoskeletonMKL1Unappreciated aspectPathwayNuclear volumeNucleoskeletonSUN2CellsActivationGenesExpression
2013
Piwi Genes Are Dispensable for Normal Hematopoiesis in Mice
Nolde MJ, Cheng EC, Guo S, Lin H. Piwi Genes Are Dispensable for Normal Hematopoiesis in Mice. PLOS ONE 2013, 8: e71950. PMID: 24058407, PMCID: PMC3751959, DOI: 10.1371/journal.pone.0071950.Peer-Reviewed Original ResearchConceptsPiwi genesHematopoietic stem cellsNormal adult hematopoiesisPIWI protein familyStem cellsStem/progenitor cellsDiverse organismsAdult hematopoiesisProtein familyLong-term hematopoiesisMyeloablative stressCompetitive transplantationTransient expressionHuman leukemia cell linesHSC compartmentLeukemia cell linesGenesProliferative stateNormal hematopoiesisCell typesMIWI2Progenitor cellsLineage reconstitutionHematopoiesisCell proliferation
2010
Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia
Raaijmakers MH, Mukherjee S, Guo S, Zhang S, Kobayashi T, Schoonmaker JA, Ebert BL, Al-Shahrour F, Hasserjian RP, Scadden EO, Aung Z, Matza M, Merkenschlager M, Lin C, Rommens JM, Scadden DT. Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia. Nature 2010, 464: 852-857. PMID: 20305640, PMCID: PMC3422863, DOI: 10.1038/nature08851.Peer-Reviewed Original ResearchConceptsSpecific mesenchymal cellsMesenchymal cellsHuman bone marrow failureDeletion of Dicer1Osteolineage cellsTissue homeostasisHeterologous cellsDicer1 deletionGene expressionMature osteoblastsRegulatory nicheBone marrow failureDiamond syndromeMesenchymal subsetsStem cellsOsteoprogenitorsReduced expressionDeletionSecondary neoplastic diseaseStromal cellsMarrow failureDICER1CellsHaematopoiesisGenetic abnormalities