2019
Stimulation of Caveolin-1 Signaling Improves Arteriovenous Fistula Patency
Hashimoto T, Isaji T, Hu H, Yamamoto K, Bai H, Santana JM, Kuo A, Kuwahara G, Foster TR, Hanisch JJ, Yatsula BA, Sessa WC, Hoshina K, Dardik A. Stimulation of Caveolin-1 Signaling Improves Arteriovenous Fistula Patency. Arteriosclerosis Thrombosis And Vascular Biology 2019, 39: 754-764. PMID: 30786746, PMCID: PMC6436985, DOI: 10.1161/atvbaha.119.312417.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, AbdominalArteriovenous Shunt, SurgicalCaveolaeCaveolin 1Cells, CulturedDrug Evaluation, PreclinicalHemorheologyHumansLungMaleMiceMice, Inbred C57BLMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIPeptide FragmentsReceptor, EphB4Signal TransductionVascular RemodelingVena Cava, InferiorConceptsCav-1 KO miceAVF maturationWT miceAVF patencyEph-B4KO miceCav-1 functionCav-1Mouse aortocaval fistula modelEphrin-B2/FcArteriovenous fistula patencyAortocaval fistula modelCaveolin-1 SignalingFistula environmentCav-1 mRNAFistula patencyHET miceVenous adaptationEndothelial cell membraneENOS activityFistula modelRC miceControl veinsWall thickeningMice
2018
CLOCK phosphorylation by AKT regulates its nuclear accumulation and circadian gene expression in peripheral tissues
Luciano AK, Zhou W, Santana JM, Kyriakides C, Velazquez H, Sessa WC. CLOCK phosphorylation by AKT regulates its nuclear accumulation and circadian gene expression in peripheral tissues. Journal Of Biological Chemistry 2018, 293: 9126-9136. PMID: 29588368, PMCID: PMC5995495, DOI: 10.1074/jbc.ra117.000773.Peer-Reviewed Original ResearchConceptsCircadian locomotor output cycles kaputCLOCK phosphorylationCircadian gene expressionPhosphorylation sitesGene expressionNovel phosphorylation sitesClock-controlled genesCRISPR/Cas9 technologyNovel Akt substrateE-box elementsCore circadian genesAkt substrateTranscription factorsE-boxCentral circadian rhythmNuclear localizationNegative regulatorCas9 technologyNuclear accumulationCircadian genesInsulin-sensitive tissuesNuclear translocationPhosphorylationExpression levelsSer-845
2016
Future research directions to improve fistula maturation and reduce access failure
Hu H, Patel S, Hanisch JJ, Santana JM, Hashimoto T, Bai H, Kudze T, Foster TR, Guo J, Yatsula B, Tsui J, Dardik A. Future research directions to improve fistula maturation and reduce access failure. Seminars In Vascular Surgery 2016, 29: 153-171. PMID: 28779782, PMCID: PMC5547899, DOI: 10.1053/j.semvascsurg.2016.08.005.Peer-Reviewed Original ResearchConceptsArteriovenous fistulaAVF maturationAVF failurePatient selectionNeointimal hyperplasiaAccess failureEnd-stage renal diseaseDrastic hemodynamic changesSetting of uremiaAppropriate patient selectionCareful patient selectionNovel interventional techniquesVascular cell activationAlternative surgical strategiesPatient-specific outcomesFistula useSystemic inflammationRenal diseaseFistula maturationInflammatory mediatorsHemodynamic changesSurgical strategyVascular accessSpecific therapyFistula anastomosisMembrane‐mediated regulation of vascular identity
Hashimoto T, Tsuneki M, Foster TR, Santana JM, Bai H, Wang M, Hu H, Hanisch JJ, Dardik A. Membrane‐mediated regulation of vascular identity. Birth Defects Research Part C Embryo Today Reviews 2016, 108: 65-84. PMID: 26992081, PMCID: PMC5310768, DOI: 10.1002/bdrc.21123.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsOrgan developmentVascular identityMembrane-associated ligandsSignal transduction pathwaysNormal organ developmentMembrane-associated moleculesEph-ephrin familyEnvironmental signalsTransduction pathwaysProper formationAberrant signalingCellular responsesDifferent cell populationsEph receptorsEphrin proteinsVessel identityElaborate coordinationSignalingVessel formationCell populationsEphDiverse pathologiesVital functionsEphrinVascular physiologyEph-B4 mediates vein graft adaptation by regulation of endothelial nitric oxide synthase
Wang M, Collins MJ, Foster TR, Bai H, Hashimoto T, Santana JM, Shu C, Dardik A. Eph-B4 mediates vein graft adaptation by regulation of endothelial nitric oxide synthase. Journal Of Vascular Surgery 2016, 65: 179-189. PMID: 26817610, PMCID: PMC4958608, DOI: 10.1016/j.jvs.2015.11.041.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsCell MovementCells, CulturedEnzyme InhibitorsEphrin-B2GenotypeHumansMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIPhenotypePhosphorylationReceptor, EphB4Saphenous VeinSignal TransductionTime FactorsVascular RemodelingVena Cava, InferiorConceptsEndothelial nitric oxide synthaseEphrin-B2/FcVein graft adaptationENOS knockout miceNitric oxide synthaseVein graftsGraft adaptationENOS phosphorylationENOS activityEph-B4Oxide synthaseKnockout miceWild-type vein graftsVessel remodelingWestern blotLess wall thickeningArginine methyl ester hydrochlorideMouse vein graftsNitric oxide productionLung endothelial cellsMouse lung endothelial cellsCell migrationLigand ephrin-B2Mechanism of actionMethyl ester hydrochloride