2023
SMAD4 maintains the fluid shear stress set point to protect against arterial-venous malformations
Banerjee K, Lin Y, Gahn J, Cordero J, Gupta P, Mohamed I, Graupera M, Dobreva G, Schwartz M, Ola R. SMAD4 maintains the fluid shear stress set point to protect against arterial-venous malformations. Journal Of Clinical Investigation 2023, 133: e168352. PMID: 37490341, PMCID: PMC10503796, DOI: 10.1172/jci168352.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriovenous MalformationsBone Morphogenetic ProteinsEndothelial CellsMiceMice, KnockoutPhosphatidylinositol 3-KinasesTelangiectasia, Hereditary HemorrhagicConceptsActivin-like kinase 1Fluid shear stressSMAD family member 4Arterial identityCyclin-dependent kinase inhibitors Cdkn2aVascular network formsEndothelial cellsVascular stabilitySensitivity of ECsBMP signalsPI3K/AktFamily member 4Downstream effectorsProtein 9Kinase 1Vascular developmentBone morphogenic protein 9Mechanism of synergyMorphological responsesSMAD4 deletionEC proliferationMember 4
2021
Defective Flow-Migration Coupling Causes Arteriovenous Malformations in Hereditary Hemorrhagic Telangiectasia
Park H, Furtado J, Poulet M, Chung M, Yun S, Lee S, Sessa WC, Franco CA, Schwartz MA, Eichmann A. Defective Flow-Migration Coupling Causes Arteriovenous Malformations in Hereditary Hemorrhagic Telangiectasia. Circulation 2021, 144: 805-822. PMID: 34182767, PMCID: PMC8429266, DOI: 10.1161/circulationaha.120.053047.Peer-Reviewed Original ResearchConceptsActivin receptor-like kinase 1Hereditary hemorrhagic telangiectasiaHemorrhagic telangiectasiaVascular malformationsArteriovenous malformationsBlood flowGrowth factor receptor 2Endothelial growth factor receptor 2Vascular endothelial growth factor receptor 2Factor receptor 2Receptor-like kinase 1New potential targetsYAP/TAZ nuclear translocationDeficient miceTransmembrane serine-threonine kinase receptorsDevastating disorderAlk1 deletionReceptor 2Pharmacologic inhibitionCre linesPostnatal retinaMalformationsSerine-threonine kinase receptorsEndothelial cell migrationNuclear translocation
2016
Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia
Baeyens N, Larrivée B, Ola R, Hayward-Piatkowskyi B, Dubrac A, Huang B, Ross TD, Coon BG, Min E, Tsarfati M, Tong H, Eichmann A, Schwartz MA. Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia. Journal Of Cell Biology 2016, 214: 807-816. PMID: 27646277, PMCID: PMC5037412, DOI: 10.1083/jcb.201603106.Peer-Reviewed Original ResearchActivin Receptors, Type IIArteriovenous MalformationsArteriovenous Shunt, SurgicalBone Morphogenetic ProteinsCell ProliferationEndoglinEndothelial CellsGene DeletionHEK293 CellsHemorheologyHuman Umbilical Vein Endothelial CellsHumansMechanotransduction, CellularPericytesRegional Blood FlowRetinaSignal TransductionSolubilityStress, MechanicalTelangiectasia, Hereditary Hemorrhagic