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
2013
AIP1 Suppresses Atherosclerosis by Limiting Hyperlipidemia-Induced Inflammation and Vascular Endothelial Dysfunction
Huang Q, Qin L, Dai S, Zhang H, Pasula S, Zhou H, Chen H, Min W. AIP1 Suppresses Atherosclerosis by Limiting Hyperlipidemia-Induced Inflammation and Vascular Endothelial Dysfunction. Arteriosclerosis Thrombosis And Vascular Biology 2013, 33: 795-804. PMID: 23413429, PMCID: PMC3637885, DOI: 10.1161/atvbaha.113.301220.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortic DiseasesApolipoproteins EAtherosclerosisBiomarkersBone Marrow TransplantationCholesterolCytokinesDisease Models, AnimalDose-Response Relationship, DrugEndothelium, VascularGene Expression RegulationHyperlipidemiasInflammationInflammation MediatorsLipoproteinsLipoproteins, LDLMacrophagesMiceMice, KnockoutNF-kappa BRas GTPase-Activating ProteinsSignal TransductionTriglyceridesVasoconstrictionVasoconstrictor AgentsVasodilationVasodilator AgentsConceptsInflammatory responseAtherosclerotic lesionsAortic ECsNuclear factor-κB (NF-κB) activityVascular endothelial dysfunctionPlasma inflammatory cytokinesWestern-type dietTotal cholesterol levelsIncreased inflammatory responseNuclear factor-κB signalingEndothelial cell dysfunctionAccumulation of macrophagesDouble knockout miceFactor-κB signalingNull mouse modelEndothelial dysfunctionProinflammatory mediatorsSuppresses AtherosclerosisControl miceInflammatory moleculesLipoprotein profileInflammatory cytokinesCholesterol levelsAortic rootEC dysfunction