2018
Decellularized materials derived from TSP2-KO mice promote enhanced neovascularization and integration in diabetic wounds
Morris AH, Stamer DK, Kunkemoeller B, Chang J, Xing H, Kyriakides TR. Decellularized materials derived from TSP2-KO mice promote enhanced neovascularization and integration in diabetic wounds. Biomaterials 2018, 169: 61-71. PMID: 29631168, PMCID: PMC5933884, DOI: 10.1016/j.biomaterials.2018.03.049.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAcellular DermisAnimalsDiabetes Mellitus, ExperimentalGene Knockdown TechniquesMiceNeovascularization, PathologicThrombospondinsTissue EngineeringTissue ScaffoldsWound HealingConceptsUltimate tensile strengthECM-based materialsTensile strengthMechanical testingDecellularized materialsElastic modulusSynthetic biomaterialsIntact slabsMatrix propertiesExtracellular matrix propertiesCell-derived ECMBiologic scaffoldsElectron microscopyEngineering controlsMaterialsWtEfficient integrationEnhanced vascularizationModulusPromigratory propertiesScaffoldsPropertiesBiomaterialsEnhanced remodelingGreater cell migration
2001
Altered Extracellular Matrix Remodeling and Angiogenesis in Sponge Granulomas of Thrombospondin 2-Null Mice
Kyriakides T, Zhu Y, Yang Z, Huynh G, Bornstein P. Altered Extracellular Matrix Remodeling and Angiogenesis in Sponge Granulomas of Thrombospondin 2-Null Mice. American Journal Of Pathology 2001, 159: 1255-1262. PMID: 11583953, PMCID: PMC1850515, DOI: 10.1016/s0002-9440(10)62512-6.Peer-Reviewed Original ResearchConceptsTSP2-null miceMatrix remodelingWild-type miceMatrix metalloproteinase-2Wild-type animalsExtracellular matrix remodelingModulators of angiogenesisFibrogenic responseImmunohistochemical analysisMetalloproteinase-2Minimal scarringMMP2 levelsSponge granulomaAngiogenesis inhibitorsMice displayVivo evidenceThrombospondin-2MiceGrowth factorImportant modulatorTissue invasionTSP2-nullWound healingAngiogenesisSignificant differencesThrombospondin‐2 plays a protective role in multistep carcinogenesis: a novel host anti‐tumor defense mechanism
Hawighorst T, Velasco P, Streit M, Hong Y, Kyriakides T, Brown L, Bornstein P, Detmar M. Thrombospondin‐2 plays a protective role in multistep carcinogenesis: a novel host anti‐tumor defense mechanism. The EMBO Journal 2001, 20: 2631-2640. PMID: 11387198, PMCID: PMC125494, DOI: 10.1093/emboj/20.11.2631.Peer-Reviewed Original ResearchMeSH Keywords9,10-Dimethyl-1,2-benzanthraceneAnimalsApoptosisCell Adhesion MoleculesCell DivisionDisease SusceptibilityEndothelial Growth FactorsFemaleGene Expression Regulation, NeoplasticLymphokinesMiceMice, Inbred StrainsMice, KnockoutNeovascularization, PathologicOligodeoxyribonucleotides, AntisensePapillomaPrecancerous ConditionsSkinSkin NeoplasmsThrombospondinsTime FactorsTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsWild-type miceTSP-2 expressionThrombospondin-2Angiogenic switchTumor formationMultistep carcinogenesisVascular endothelial growth factorAnti-angiogenic factorsTSP-2-deficient miceEndothelial growth factorAngiogenesis inhibitor thrombospondin-2Endogenous angiogenesis inhibitorTumor cell apoptosisTumor differentiationMesenchymal stromaMulti-step tumorigenesisDefense mechanismsAngiogenesis inhibitorsProtective roleAngiogenesis factorsTumor angiogenesisTumor cellsGrowth factorCell apoptosisRegulation of Angiogenesis and Matrix Remodeling by Localized, Matrix-Mediated Antisense Gene Delivery
Kyriakides T, Hartzel T, Huynh G, Bornstein P. Regulation of Angiogenesis and Matrix Remodeling by Localized, Matrix-Mediated Antisense Gene Delivery. Molecular Therapy 2001, 3: 842-849. PMID: 11407897, DOI: 10.1006/mthe.2001.0336.Peer-Reviewed Original Research
1999
Mice that lack the angiogenesis inhibitor, thrombospondin 2, mount an altered foreign body reaction characterized by increased vascularity
Kyriakides T, Leach K, Hoffman A, Ratner B, Bornstein P. Mice that lack the angiogenesis inhibitor, thrombospondin 2, mount an altered foreign body reaction characterized by increased vascularity. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 4449-4454. PMID: 10200282, PMCID: PMC16352, DOI: 10.1073/pnas.96.8.4449.Peer-Reviewed Original Research