2021
Human-Induced Pluripotent Stem-Cell-Derived Smooth Muscle Cells Increase Angiogenesis to Treat Hindlimb Ischemia
Gao X, Gao M, Gorecka J, Langford J, Liu J, Luo J, Taniguchi R, Matsubara Y, Liu H, Guo L, Gu Y, Qyang Y, Dardik A. Human-Induced Pluripotent Stem-Cell-Derived Smooth Muscle Cells Increase Angiogenesis to Treat Hindlimb Ischemia. Cells 2021, 10: 792. PMID: 33918299, PMCID: PMC8066461, DOI: 10.3390/cells10040792.Peer-Reviewed Original ResearchConceptsLimb-threatening ischemiaSmooth muscle cellsHindlimb ischemiaFunctional outcomeChronic limb-threatening ischemiaMuscle cellsVascular endothelial growth factor (VEGF) expressionM2-type macrophagesMurine hindlimb ischemia modelNumber of macrophagesGrowth factor expressionLaser Doppler imagingStem cell sourceHindlimb ischemia modelStem cellsConsiderable ethical issuesTranslatable therapyIschemic limbsRenewable stem cell sourcesIschemia modelCapillary densityBlood flowIschemiaNovel treatmentsNude mice
2019
Modular design of a tissue engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes
Park J, Anderson CW, Sewanan LR, Kural MH, Huang Y, Luo J, Gui L, Riaz M, Lopez CA, Ng R, Das SK, Wang J, Niklason L, Campbell SG, Qyang Y. Modular design of a tissue engineered pulsatile conduit using human induced pluripotent stem cell-derived cardiomyocytes. Acta Biomaterialia 2019, 102: 220-230. PMID: 31634626, PMCID: PMC7227659, DOI: 10.1016/j.actbio.2019.10.019.Peer-Reviewed Original ResearchConceptsSingle-ventricle cardiac defectsHuman umbilical arteryPluripotent stem cell-derived cardiomyocytesStem cell-derived cardiomyocytesFontan procedureSurgical interventionSVD patientsCell-derived cardiomyocytesFontan conduitTherapeutic potentialEngineered Heart TissueVascular conduitsCongenital disorderDesign strategyVariety of complicationsEfficient electrical conductivitySingle ventricle heartPrimary cardiac fibroblastsFontan circulationHeart failureCorrective surgeryUmbilical arteryPulmonary circulationBiodegradable materialsPulmonary systemPatient mutations linked to arrhythmogenic cardiomyopathy enhance calpain-mediated desmoplakin degradation
Ng R, Manring H, Papoutsidakis N, Albertelli T, Tsai N, See CJ, Li X, Park J, Stevens TL, Bobbili PJ, Riaz M, Ren Y, Stoddard CE, Janssen PM, Bunch TJ, Hall SP, Lo YC, Jacoby DL, Qyang Y, Wright N, Ackermann MA, Campbell SG. Patient mutations linked to arrhythmogenic cardiomyopathy enhance calpain-mediated desmoplakin degradation. JCI Insight 2019, 5 PMID: 31194698, PMCID: PMC6675562, DOI: 10.1172/jci.insight.128643.Peer-Reviewed Original Research
2016
Implantable tissue-engineered blood vessels from human induced pluripotent stem cells
Gui L, Dash BC, Luo J, Qin L, Zhao L, Yamamoto K, Hashimoto T, Wu H, Dardik A, Tellides G, Niklason LE, Qyang Y. Implantable tissue-engineered blood vessels from human induced pluripotent stem cells. Biomaterials 2016, 102: 120-129. PMID: 27336184, PMCID: PMC4939127, DOI: 10.1016/j.biomaterials.2016.06.010.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsVascular diseaseBlood vesselsAlpha-smooth muscle actinSmooth muscle myosin heavy chainActive vascular remodelingSmooth muscle cellsMuscle myosin heavy chainTissue-engineered blood vesselsStem cellsAbundant collagenous matrixPluripotent stem cellsInterposition graftAllogeneic graftsVascular remodelingΑ-SMANude ratsMuscle actinMyosin heavy chainClinical useMuscle cellsFunctional vascular smooth muscle cellsPatientsFunctional tissue-engineered blood vesselGraft
2007
The Renewal and Differentiation of Isl1 + Cardiovascular Progenitors Are Controlled by a Wnt/β-Catenin Pathway
Qyang Y, Martin-Puig S, Chiravuri M, Chen S, Xu H, Bu L, Jiang X, Lin L, Granger A, Moretti A, Caron L, Wu X, Clarke J, Taketo MM, Laugwitz KL, Moon RT, Gruber P, Evans SM, Ding S, Chien KR. The Renewal and Differentiation of Isl1 + Cardiovascular Progenitors Are Controlled by a Wnt/β-Catenin Pathway. Cell Stem Cell 2007, 1: 165-179. PMID: 18371348, DOI: 10.1016/j.stem.2007.05.018.Peer-Reviewed Original Research
2004
Myeloproliferative Disease in Mice with Reduced Presenilin Gene Dosage: Effect of γ-Secretase Blockage †
Qyang Y, Chambers SM, Wang P, Xia X, Chen X, Goodell MA, Zheng H. Myeloproliferative Disease in Mice with Reduced Presenilin Gene Dosage: Effect of γ-Secretase Blockage †. Biochemistry 2004, 43: 5352-5359. PMID: 15122901, DOI: 10.1021/bi049826u.Peer-Reviewed Original ResearchMeSH KeywordsAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesCell LineageColony-Forming Units AssayEndopeptidasesFemaleGene DosageGranulocytesHematopoiesisLeukocyte CountMacrophagesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMyeloproliferative DisordersPresenilin-1Presenilin-2Protease InhibitorsConceptsGamma-secretase activityDisease interventionWild-type splenocytesAlzheimer's disease interventionsAmyloid precursor proteinGranulocyte-macrophage colony-forming unitsGamma-secretase inhibitorsGamma-secretase cleavageGranulocyte infiltrationPotential therapyMyeloproliferative diseaseB lymphocytesBone marrowPS inactivationHematopoietic stem cellsColony-forming unitsGranulocytic cells