2024
Loss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis
Dave J, Chakraborty R, Agyemang A, Ntokou A, Saito J, Ballabh P, Martin K, Greif D. Loss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis. Stroke 2024, 55: 2340-2352. PMID: 39129597, PMCID: PMC11347087, DOI: 10.1161/strokeaha.123.045248.Peer-Reviewed Original ResearchAngiopoietin-2Germinal matrix hemorrhage-intraventricular hemorrhagePerinatal lethalityEndothelial cell hyperproliferationEndothelial cellsBrain pericytesGenetic inhibitionVascular cellsBlood-brain barrier integrityBlood-brain barrier developmentBrain vascular cellsAbnormal vessel morphologyVessel morphologyProlonged survivalRegulating cross-talkMutant endothelial cellsHuman brain pericytesGerminal matrixCell hyperproliferationPhosphorylates Tie2Embryonic miceCellular sourceBarrier integrityGenetic ablationTherapeutic effect
2023
TNFα increases the degradation of pyruvate dehydrogenase kinase 4 by the Lon protease to support proinflammatory genes
Boutagy N, Fowler J, Grabinska K, Cardone R, Sun Q, Vazquez K, Whalen M, Zhu X, Chakraborty R, Martin K, Simons M, Romanoski C, Kibbey R, Sessa W. TNFα increases the degradation of pyruvate dehydrogenase kinase 4 by the Lon protease to support proinflammatory genes. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2218150120. PMID: 37695914, PMCID: PMC10515159, DOI: 10.1073/pnas.2218150120.Peer-Reviewed Original ResearchConceptsPyruvate dehydrogenase kinase 4Dehydrogenase kinase 4Lon proteasePyruvate dehydrogenase activityHistone acetylationMitochondrial metabolismKinase 4Specific gene lociPDH fluxEndothelial cellsSiRNA-mediated knockdownAcetyl-CoA generationLysine 27Gene transcriptionTCA fluxRNA sequencingHuman umbilical vein endothelial cellsProtein degradationHistone 3Gene locusUmbilical vein endothelial cellsNF-κB-dependent mechanismTricarboxylic acid cycle fluxVein endothelial cellsActive subunit
2010
6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle
Martin K, Rzucidlo E, Ding M, Merenick B, Kasza Z, Wagner R, Powell R. 6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle. 2010, 69-96. DOI: 10.1016/b978-0-08-046884-6.00705-3.ChaptersVascular smooth muscle cellsPhenotypic modulationInsulin-like growth factor IEndothelial cellsVSMC differentiationPathogenesis of atherosclerosisRapamycin (mTOR) inhibitor rapamycinSerum response factorDedifferentiated vascular smooth muscle cellsGrowth factor INormal vascular physiologyActivated T cellsSmooth muscle cellsContractile protein expressionEffects of drugsT cellsSmooth muscleIntimal hyperplasiaFactor family membersTumor angiogenesisVascular physiologyMature arteriesFactor IMuscle cellsVSMC phenotype
2009
Adiponectin Induces Vascular Smooth Muscle Cell Differentiation via AMPK
Ding M, Wagner R, Fetalvero K, Kasza Z, Powell R, Martin K. Adiponectin Induces Vascular Smooth Muscle Cell Differentiation via AMPK. The FASEB Journal 2009, 23: 577.10-577.10. DOI: 10.1096/fasebj.23.1_supplement.577.10.Peer-Reviewed Original ResearchMTOR inhibitionLower adiponectin levelsVSMC differentiationType 2 diabetesVascular smooth muscle cell phenotypeSmooth muscle cell phenotypeAMPK activationDose-dependent mannerContractile protein expressionAMPK inhibitor compound C.Muscle cell phenotypeVascular smooth muscle cell differentiationVSMC contractile phenotypeAdipo-R1Smooth muscle cell differentiationAdiponectin levelsSerum hormonesCardioprotective roleHormonal inhibitorCardiovascular diseaseAdiponectinCardioprotective functionControl virusEndothelial cellsVSMC
2005
Endothelial cell activation of the smooth muscle cell phosphoinositide 3-kinase/Akt pathway promotes differentiation
Brown D, Rzucidlo E, Merenick B, Wagner R, Martin K, Powell R. Endothelial cell activation of the smooth muscle cell phosphoinositide 3-kinase/Akt pathway promotes differentiation. Journal Of Vascular Surgery 2005, 41: 509-516. PMID: 15838487, DOI: 10.1016/j.jvs.2004.12.024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, ThoracicCattleCell DifferentiationCells, CulturedCoculture TechniquesEndothelial CellsMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypePhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionConceptsEC/SMCDifferentiated SMC phenotypeSMC phenotypeSMC differentiationSmooth muscle cellsAkt pathwayProtein markersProtein kinase AktAdenoviral overexpressionContractile protein markersDominant-negative AktEndothelial cellsOpposite endothelial cellsBlood vessel developmentRapid Akt phosphorylationPI3K/Akt pathwayMuscle cellsWestern blottingKinase AktAbility of ECsActive AktPhosphoinositide 3Kinase activityMolecular signalsSynthetic phenotype