2023
An optimized visualization and quantitative protocol for in-depth evaluation of lymphatic vessel architecture in the liver
Jeong J, Tanaka M, Yang Y, Arefyev N, DiRito J, Tietjen G, Zhang X, McConnell M, Utsumi T, Iwakiri Y. An optimized visualization and quantitative protocol for in-depth evaluation of lymphatic vessel architecture in the liver. AJP Gastrointestinal And Liver Physiology 2023, 325: g379-g390. PMID: 37605828, PMCID: PMC10887843, DOI: 10.1152/ajpgi.00139.2023.Peer-Reviewed Original Research
2021
Alcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease
Yang Y, Sangwung P, Kondo R, Jung Y, McConnell MJ, Jeong J, Utsumi T, Sessa WC, Iwakiri Y. Alcohol-induced Hsp90 acetylation is a novel driver of liver sinusoidal endothelial dysfunction and alcohol-related liver disease. Journal Of Hepatology 2021, 75: 377-386. PMID: 33675874, PMCID: PMC8292196, DOI: 10.1016/j.jhep.2021.02.028.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseAlcohol-induced liver injuryLiver sinusoidal endothelial cellsAlcohol-related liver diseaseLiver injuryLSEC dysfunctionHsp90 acetylationNO productionHistone deacetylase 6Liver diseaseTherapeutic strategiesHeat shock protein 90 (Hsp90) acetylationLiver sinusoidal endothelial dysfunctionSinusoidal endothelial cell dysfunctionMouse liver sinusoidal endothelial cellsEndothelial cell dysfunctionNitric oxide synthaseEthanol-fed miceSinusoidal endothelial dysfunctionPotential therapeutic approachPotential therapeutic strategyNitric oxide productionNew therapeutic strategiesSinusoidal endothelial cellsAcetylation of Hsp90
2020
Single-Cell Transcriptomics Reveals Zone-Specific Alterations of Liver Sinusoidal Endothelial Cells in Cirrhosis
Su T, Yang Y, Lai S, Jeong J, Jung Y, McConnell M, Utsumi T, Iwakiri Y. Single-Cell Transcriptomics Reveals Zone-Specific Alterations of Liver Sinusoidal Endothelial Cells in Cirrhosis. Cellular And Molecular Gastroenterology And Hepatology 2020, 11: 1139-1161. PMID: 33340713, PMCID: PMC7903131, DOI: 10.1016/j.jcmgh.2020.12.007.Peer-Reviewed Original ResearchConceptsLiver sinusoidal endothelial cellsCirrhotic miceSinusoidal endothelial cellsLiver cirrhosisEndothelial cellsIntrahepatic vascular resistanceCarbon tetrachloride inhalationNovel therapeutic strategiesNitric oxide productionCirrhotic mouse liverEC populationsVascular resistanceClinical complicationsLiver fibrosisTherapeutic strategiesCirrhosisOxide productionEndocytic receptorMiceAbstractTextZone 3Extracellular matrix genesVascular ECsLymphatic ECsMouse liver
2018
Astragaloside IV reduces neuronal apoptosis and parthanatos in ischemic injury by preserving mitochondrial hexokinase-II
Li Y, Yang Y, Zhao Y, Zhang J, Liu B, Jiao S, Zhang X. Astragaloside IV reduces neuronal apoptosis and parthanatos in ischemic injury by preserving mitochondrial hexokinase-II. Free Radical Biology And Medicine 2018, 131: 251-263. PMID: 30502455, DOI: 10.1016/j.freeradbiomed.2018.11.033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Inducing FactorAstragalus propinquusFemaleGene Expression RegulationGlutamic AcidHexokinaseHumansHypoxia-Ischemia, BrainInfarction, Middle Cerebral ArteryMembrane Potential, MitochondrialMiceMice, Inbred C57BLMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNeuronsNeuroprotective AgentsOxygen ConsumptionParthanatosPrimary Cell CultureProtein BindingProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySaponinsTriterpenesConceptsMitochondrial hexokinase-IIApoptosis inducing factorHexokinase-IIRelease of pro-apoptotic proteinsNuclear translocation of apoptosis inducing factorTranslocation of apoptosis inducing factorCollapse of mitochondrial membrane potentialMitochondrial dysfunctionFunctional integrity of mitochondriaMitochondrial permeability transition porePro-apoptotic proteinsBinding to mitochondriaDNA damageIntegrity of mitochondriaMitochondrial membrane potentialPermeability transition poreImpaired mitochondrial functionSimultaneously induced apoptosisNeuronal cell deathTransition porePAR formationMitochondrial functionParthanatosCell deathMitochondria