2020
Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis
Li J, Huynh L, Cornwell WD, Tang MS, Simborio H, Huang J, Kosmider B, Rogers TJ, Zhao H, Steinberg MB, Thu Thi Le L, Zhang L, Pham K, Liu C, Wang H. Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis. Arteriosclerosis Thrombosis And Vascular Biology 2020, 41: 839-853. PMID: 33380174, PMCID: PMC8608030, DOI: 10.1161/atvbaha.120.315556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAtherosclerosisDisease Models, AnimalDNA DamageDNA, MitochondrialE-Cigarette VaporFemaleHumansInflammationInflammation MediatorsMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout, ApoEMiddle AgedMitochondriaRAW 264.7 CellsSignal TransductionSmokersToll-Like Receptor 9VapingConceptsECV exposureTLR9 expressionInflammatory cytokinesClassical monocytesTLR9 activationAtherosclerotic plaquesEight-week-old ApoEUpregulation of TLR9Expression of TLR9Atherosclerotic lesion developmentOil Red O stainingToll-like receptorsDays/weekE-cig exposureMonocytes/macrophagesNormal laboratory dietRed O stainingPotential pharmacological targetElectronic cigarette useHours/dayProinflammatory cytokinesCig vaporPlasma levelsTLR9 antagonistTLR9 inhibitorE-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1
Pham K, Huynh D, Le L, Delitto D, Yang L, Huang J, Kang Y, Steinberg MB, Li J, Zhang L, Liu D, Tang MS, Liu C, Wang H. E-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1. Cancer Letters 2020, 491: 132-145. PMID: 32829009, PMCID: PMC9703643, DOI: 10.1016/j.canlet.2020.08.010.Peer-Reviewed Original ResearchConceptsBC cell growthCig exposureLung metastasesBreast cancerVCAM-1V-CAM-1Role of CCL5Upregulated protein expressionBC cell survivalE-cig exposurePro-tumorigenic factorsBC cell apoptosisBreast carcinoma progressionMetastatic lung colonizationCCR5 axisMFP tumorsTAMs infiltrationInfiltrated macrophagesCell growthCo-culture systemImmunohistochemical stainsCell crosstalkBC cellsBC growthProliferation indexThe role of survivin in the progression of pancreatic ductal adenocarcinoma (PDAC) and a novel survivin-targeted therapeutic for PDAC
Brown M, Zhang W, Yan D, Kenath R, Le L, Wang H, Delitto D, Ostrov D, Robertson K, Liu C, Pham K. The role of survivin in the progression of pancreatic ductal adenocarcinoma (PDAC) and a novel survivin-targeted therapeutic for PDAC. PLOS ONE 2020, 15: e0226917. PMID: 31929540, PMCID: PMC6957139, DOI: 10.1371/journal.pone.0226917.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTypes of cancerDuctal adenocarcinomaSurvivin expressionSurvivin inhibitorClinical response rateNovel survivin inhibitorHalf of patientsElevated survivin expressionLower patient survivalPancreatic tumor microenvironmentPotential therapeutic targetExpression of survivinRole of survivinField of oncologyPancreatic cancer linesImmunotherapeutic approachesPatient survivalUntreated cohortTherapeutic responseInhibitor of survivinTreatment resistancePDAC progressionEffective treatmentTumor cell migration
2013
Altered vascular activation due to deficiency of the NADPH oxidase component p22phox
Wang H, Albadawi H, Siddiquee Z, Stone J, Panchenko M, Watkins M, Stone J. Altered vascular activation due to deficiency of the NADPH oxidase component p22phox. Cardiovascular Pathology 2013, 23: 35-42. PMID: 24035466, DOI: 10.1016/j.carpath.2013.08.003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarotid Artery InjuriesCarotid Artery, CommonCase-Control StudiesCasein Kinase IalphaCells, CulturedCoronary VesselsCytochrome b GroupElastic TissueFemaleGranulomatous Disease, ChronicHeterogeneous-Nuclear Ribonucleoprotein Group CHumansHyperplasiaInfantMaleMatrix Metalloproteinase 12MiceMice, KnockoutMuscle, Smooth, VascularNADPH OxidasesNeointimaReactive Oxygen SpeciesRNA InterferenceTissue Inhibitor of Metalloproteinase-1TransfectionConceptsWild-type littermatesElastic fiber lossVascular activationDeficient miceIntimal hyperplasiaNADPH oxidase complexCoronary artery smooth muscle cellsNicotinamide adenine dinucleotide phosphate (NADPH) oxidaseArtery smooth muscle cellsHuman coronary artery smooth muscle cellsAdenine Dinucleotide Phosphate OxidaseBasal blood pressureCarotid artery ligationExpression ratioSmooth muscle cellsLung biopsyBlood pressureFiber lossArtery ligationCarotid ligationCarotid arteryTissue inhibitorHuman patientsMuscle cellsMice
2012
SEC23B is required for the maintenance of murine professional secretory tissues
Tao J, Zhu M, Wang H, Afelik S, Vasievich M, Chen X, Zhu G, Jensen J, Ginsburg D, Zhang B. SEC23B is required for the maintenance of murine professional secretory tissues. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: e2001-e2009. PMID: 22745161, PMCID: PMC3406820, DOI: 10.1073/pnas.1209207109.Peer-Reviewed Original ResearchMeSH KeywordsAlcian BlueAnimalsAnthraquinonesApoptosisEndoplasmic ReticulumFluorescent Antibody TechniqueHumansIn Situ Nick-End LabelingMiceMice, Inbred C57BLMice, TransgenicMicroscopy, ImmunoelectronMutationPancreasReal-Time Polymerase Chain ReactionSecretory PathwaySpecies SpecificityVesicular Transport ProteinsConceptsEndoplasmic reticulumSecretory tissueSpecies-specific shiftsGTPase-activating proteinsUnfolded protein responseAccumulation of proteinsSimilar ultrastructural alterationsAbundant cargoCargo recognitionEukaryotic cellsSar1 GTPaseER exitER lumenSecretory pathwayTissue-specific dependenceProtein responseHypomorphic mutationsSecretory proteinsSEC23BDisparate phenotypesCOPIICongenital dyserythropoietic anemia type IIEmbryonic pancreasAnemia phenotypeProapoptotic pathways
2008
Transgenic overexpression of a stable Plasminogen Activator Inhibitor-1 variant
Fahim A, Wang H, Feng J, Ginsburg D. Transgenic overexpression of a stable Plasminogen Activator Inhibitor-1 variant. Thrombosis Research 2008, 123: 785-792. PMID: 18774162, PMCID: PMC2670886, DOI: 10.1016/j.thromres.2008.07.004.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Plasma PAI-1 levelsPAI-1 levelsPAI-1 mRNAHigher plasma PAI-1 levelsTransgenic overexpressionEvidence of thrombosisActivator inhibitor-1PAI-1 variantsApparent thrombosisHistologic examinationSerine protease inhibitor gene familyPhysiologic effectsTransgenic miceChicken beta-actin promoterModerate expressionInhibitor-1High expressionBeta-actin promoterBiologic importanceThrombosisPhysiologic conditionsKidneyMiceLiver