2015
ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy
Albright RA, Stabach P, Cao W, Kavanagh D, Mullen I, Braddock AA, Covo MS, Tehan M, Yang G, Cheng Z, Bouchard K, Yu ZX, Thorn S, Wang X, Folta-Stogniew EJ, Negrete A, Sinusas AJ, Shiloach J, Zubal G, Madri JA, De La Cruz EM, Braddock DT. ENPP1-Fc prevents mortality and vascular calcifications in rodent model of generalized arterial calcification of infancy. Nature Communications 2015, 6: 10006. PMID: 26624227, PMCID: PMC4686714, DOI: 10.1038/ncomms10006.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseVascular calcificationArterial calcificationOrphan diseaseCommon diseaseSequelae of diseaseEctopic vascular calcificationInternal elastic laminaPrevent mortalityRenal failureCardiac failureKidney diseaseSubcutaneous administrationRodent modelsAnimal modelsEctopic calcificationVascular wallLarge arteriesElastic laminaDiseaseCalcificationCalciphylaxisDecreased concentrationSclerosisArteryDeletion 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 stressPET imaging of a collagen matrix reveals its effective injection and targeted retention in a mouse model of myocardial infarction
Ahmadi A, Thorn SL, Alarcon EI, Kordos M, Padavan DT, Hadizad T, Cron GO, Beanlands RS, DaSilva JN, Ruel M, deKemp RA, Suuronen EJ. PET imaging of a collagen matrix reveals its effective injection and targeted retention in a mouse model of myocardial infarction. Biomaterials 2015, 49: 18-26. PMID: 25725551, DOI: 10.1016/j.biomaterials.2015.01.016.Peer-Reviewed Original ResearchConceptsMyocardial infarctionPositron emission tomographyPET imagingMouse modelNon-invasive PET imagingCardiac regeneration therapyIschemic territoryPET resultsInfarcted myocardiumEmission tomographyCollagen matrixMyocardial injectionEarly retentionPromising modalityRegeneration therapyInfarctionLabeling efficiencyMyocardiumFluorescence imagingImagingBiodistributionInjectionQdot labelingEx
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