2021
ATPIF1 maintains normal mitochondrial structure which is impaired by CCM3 deficiency in endothelial cells
Wang K, Chen H, Zhou Z, Zhang H, Zhou HJ, Min W. ATPIF1 maintains normal mitochondrial structure which is impaired by CCM3 deficiency in endothelial cells. Cell & Bioscience 2021, 11: 11. PMID: 33422124, PMCID: PMC7796565, DOI: 10.1186/s13578-020-00514-z.Peer-Reviewed Original ResearchActivation of mitophagyHuman umbilical vein endothelial cellsNormal mitochondrial structureMorphology of mitochondriaRNA-seq screeningMitochondrial membrane potentialCRISPR-Cas9 SystemCerebral cavernous malformationsEndothelial cellsExpression of KLF4Destruction of mitochondriaUmbilical vein endothelial cellsMitochondrial structureSignaling pathwaysVein endothelial cellsMitochondriaATPIF1MitophagyEndothelial progenitor cellsProgenitor cellsCell proliferationMembrane potentialKLF4PathwayProtein
2017
Lead promotes abnormal angiogenesis induced by CCM3 gene defects via mitochondrial pathway
Sun Y, Zhang H, Xing X, Zhao Z, He J, Li J, Chen J, Wang M, He Y. Lead promotes abnormal angiogenesis induced by CCM3 gene defects via mitochondrial pathway. Journal Of Developmental Origins Of Health And Disease 2017, 9: 182-190. PMID: 29110746, DOI: 10.1017/s2040174417000782.Peer-Reviewed Original ResearchConceptsMouse embryosYolk sacHeterozygous mouse embryosGene defectsCCM3 genesPrimary human umbilical vein endothelial cellsLead exposureMitochondrial DNAEmbryonic developmentMtDNA biogenesisMitochondrial morphologyCardiovascular developmentHuman umbilical vein endothelial cellsMitochondrial pathwayGene knockoutEndothelial cellsUmbilical vein endothelial cellsVascular developmentMitochondria pathwayVein endothelial cellsPrimary cellsGenesRNA expressionCell proliferationEmbryos
2011
AIP1 Prevents Graft Arteriosclerosis by Inhibiting Interferon-&ggr;–Dependent Smooth Muscle Cell Proliferation and Intimal Expansion
Yu L, Qin L, Zhang H, He Y, Chen H, Pober JS, Tellides G, Min W. AIP1 Prevents Graft Arteriosclerosis by Inhibiting Interferon-&ggr;–Dependent Smooth Muscle Cell Proliferation and Intimal Expansion. Circulation Research 2011, 109: 418-427. PMID: 21700930, PMCID: PMC3227522, DOI: 10.1161/circresaha.111.248245.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, AbdominalAorta, ThoracicArteriosclerosisCell MovementCell ProliferationCells, CulturedDisease Models, AnimalHumansInterferon-gammaJanus Kinase 2MaleMiceMice, KnockoutMinor Histocompatibility AntigensMuscle, Smooth, VascularRas GTPase-Activating ProteinsReceptors, InterferonSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTime FactorsTunica IntimaVascular GraftingConceptsASK1-interacting protein-1Neointima formationTransplantation modelIntimal expansionSingle minor histocompatibility antigenSmooth muscle cell proliferationMinor histocompatibility antigensAortic transplantation modelAorta transplantation modelMuscle cell proliferationVSMC accumulationDonor graftsGraft arteriosclerosisIntimal formationIntravenous administrationHistocompatibility antigensVSMC proliferationMouse aortaVSMC migrationIFNProliferative diseasesEndothelial cellsProtein 1Cell proliferationJAK-STAT signaling