2022
Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation
Su KN, Ma Y, Cacheux M, Ilkan Z, Raad N, Muller GK, Wu X, Guerrera N, Thorn SL, Sinusas AJ, Foretz M, Viollet B, Akar JG, Akar FG, Young LH. Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation. JCI Insight 2022, 7: e141213. PMID: 35451373, PMCID: PMC9089788, DOI: 10.1172/jci.insight.141213.Peer-Reviewed Original ResearchConceptsTranscription factorsKey transcription factorMaster metabolic regulatorIon channel subunitsGap junction proteinTranscriptional reprogrammingAMPK deletionProtein kinaseBiological functionsTranscriptional downregulationMetabolic regulatorChannel subunitsIon channelsAMPK expressionMetabolic stressAtrial fibrillationAMPKJunction proteinsElectrical excitabilityHomeostatic roleStructural remodelingConnexinsAtrial ion channelsRemodelingDownregulation
2015
Deletion of MLIP (Muscle-enriched A-type Lamin-interacting Protein) Leads to Cardiac Hyperactivation of Akt/Mammalian Target of Rapamycin (mTOR) and Impaired Cardiac Adaptation*
Cattin ME, Wang J, Weldrick JJ, Roeske CL, Mak E, Thorn SL, DaSilva JN, Wang Y, Lusis AJ, Burgon PG. Deletion of MLIP (Muscle-enriched A-type Lamin-interacting Protein) Leads to Cardiac Hyperactivation of Akt/Mammalian Target of Rapamycin (mTOR) and Impaired Cardiac Adaptation*. Journal Of Biological Chemistry 2015, 290: 26699-26714. PMID: 26359501, PMCID: PMC4646324, DOI: 10.1074/jbc.m115.678433.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsCardiomegalyCarrier ProteinsCo-Repressor ProteinsFemaleGene Expression RegulationGenome-Wide Association StudyHeart Function TestsHemodynamicsIsoproterenolMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacNuclear ProteinsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionStress, PhysiologicalTOR Serine-Threonine KinasesUltrasonographyConceptsAKT/mTOR pathwayGenome-wide association studiesAkt/mammalian targetMTOR pathwayAkt/mTOR activityAkt/mTORUnique proteinsUnknown functionAssociation studiesMTOR activityMammalian targetCardiac adaptationRegenerative abilityGenetic associationAdult heartPathwayHomeostasisMyocardial metabolic abnormalitiesNormal cardiac functionAdaptationEarly responseMetabolic abnormalitiesCardiac functionMLIPCardiac stress
2014
Glutaredoxin-2 Is Required to Control Oxidative Phosphorylation in Cardiac Muscle by Mediating Deglutathionylation Reactions*
Mailloux RJ, Xuan JY, McBride S, Maharsy W, Thorn S, Holterman CE, Kennedy CR, Rippstein P, deKemp R, da Silva J, Nemer M, Lou M, Harper ME. Glutaredoxin-2 Is Required to Control Oxidative Phosphorylation in Cardiac Muscle by Mediating Deglutathionylation Reactions*. Journal Of Biological Chemistry 2014, 289: 14812-14828. PMID: 24727547, PMCID: PMC4031535, DOI: 10.1074/jbc.m114.550574.Peer-Reviewed Original ResearchThe role of integrin α2 in cell and matrix therapy that improves perfusion, viability and function of infarcted myocardium
Ahmadi A, McNeill B, Vulesevic B, Kordos M, Mesana L, Thorn S, Renaud JM, Manthorp E, Kuraitis D, Toeg H, Mesana TG, Davis DR, Beanlands RS, DaSilva JN, deKemp RA, Ruel M, Suuronen EJ. The role of integrin α2 in cell and matrix therapy that improves perfusion, viability and function of infarcted myocardium. Biomaterials 2014, 35: 4749-4758. PMID: 24631247, DOI: 10.1016/j.biomaterials.2014.02.028.Peer-Reviewed Original ResearchConceptsMatrix therapyMouse myocardial infarction modelMyocardial infarction modelCardiac cell therapySynergistic therapeutic effectTherapeutic effectMyocardial perfusionParacrine propertiesInfarcted myocardiumAngiogenic cellsInfarction modelOverall efficacyTherapyCell therapyAngiogenic potentialCACSΑ5 integrinIntegrin α2EngraftmentIntegrin α5PerfusionCellsIntegrinsCollagen matrixCAC function
2013
Repeatable Noninvasive Measurement of Mouse Myocardial Glucose Uptake with 18F-FDG: Evaluation of Tracer Kinetics in a Type 1 Diabetes Model
Thorn SL, deKemp RA, Dumouchel T, Klein R, Renaud JM, Wells RG, Gollob MH, Beanlands RS, DaSilva JN. Repeatable Noninvasive Measurement of Mouse Myocardial Glucose Uptake with 18F-FDG: Evaluation of Tracer Kinetics in a Type 1 Diabetes Model. Journal Of Nuclear Medicine 2013, 54: 1637-1644. PMID: 23940301, DOI: 10.2967/jnumed.112.110114.Peer-Reviewed Original ResearchConceptsMyocardial glucose uptakeImage-derived blood input functionAcute insulin treatmentInsulin treatmentBlood activityType 1 diabetic miceType 1 diabetic mouse modelML/min/Glucose uptakeVena cava diameterMyocardial glucose uptake ratesDiabetic mouse modelType 1 diabetesStandardized uptake valueTest-retest repeatabilityAcute insulin stimulationDiabetic miceCoefficient of repeatabilityFDG-PETBland-Altman analysisMyocardial glucoseContrast CTBaseline scanMouse modelTime-activity curvesMicroRNA-133 Controls Brown Adipose Determination in Skeletal Muscle Satellite Cells by Targeting Prdm16
Yin H, Pasut A, Soleimani VD, Bentzinger CF, Antoun G, Thorn S, Seale P, Fernando P, van IJcken W, Grosveld F, Dekemp RA, Boushel R, Harper ME, Rudnicki MA. MicroRNA-133 Controls Brown Adipose Determination in Skeletal Muscle Satellite Cells by Targeting Prdm16. Cell Metabolism 2013, 17: 210-224. PMID: 23395168, PMCID: PMC3641657, DOI: 10.1016/j.cmet.2013.01.004.Peer-Reviewed Original ResearchMeSH Keywords3' Untranslated RegionsAdipocytes, BrownAdipose Tissue, BrownAnimalsBase SequenceCell DifferentiationCell LineageCold TemperatureDNA-Binding ProteinsDown-RegulationEnergy MetabolismGlucose Tolerance TestMiceMicroRNAsMolecular Sequence DataMultipotent Stem CellsRegenerationSatellite Cells, Skeletal MuscleTranscription FactorsConceptsAdult skeletal muscle stem cellsSkeletal muscle stem cellsBrown adipocytesSkeletal muscle satellite cellsMuscle stem cellsSatellite cellsAdult satellite cellsLineage-tracing experimentsMuscle satellite cellsMyogenic lineageEmbryonic developmentMyogenic progenitorsMicroRNA-133De novo generationMiR-133 levelsBrown adipose tissueWhole-body energy expenditureMuscle regenerationUncoupled respirationEnergy metabolismStem cellsImportant therapeutic targetNovo generationThermogenic tissuesGlucose uptake
2012
A three-dimensional model-based partial volume correction strategy for gated cardiac mouse PET imaging
Dumouchel T, Thorn S, Kordos M, DaSilva J, Beanlands RS, deKemp RA. A three-dimensional model-based partial volume correction strategy for gated cardiac mouse PET imaging. Physics In Medicine And Biology 2012, 57: 4309-4334. PMID: 22705820, DOI: 10.1088/0031-9155/57/13/4309.Peer-Reviewed Original Research
2009
Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen
Folmes KD, Chan AY, Koonen DP, Pulinilkunnil TC, Baczkó I, Hunter BE, Thorn S, Allard MF, Roberts R, Gollob MH, Light PE, Dyck JR. Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen. Circulation Genomic And Precision Medicine 2009, 2: 457-466. PMID: 20031621, DOI: 10.1161/circgenetics.108.834564.Peer-Reviewed Original ResearchConceptsTransgenic miceR302Q mutationGlycogen contentAcute expressionCardiomyocyte-restricted expressionAMPK activationTransgenic adult miceNeonatal rat cardiomyocytesChronic modelWolff-ParkinsonGlycogen synthase activityWhite syndromeCardiac hypertrophyAdult miceGlycogen storage cardiomyopathyMyocardial glycogenDirect effectCompensatory alterationsRat cardiomyocytesFamilial formsMiceEarly signaling eventCardiomyopathyAMPK activityHeart