2023
Very-long-chain fatty acids induce glial-derived sphingosine-1-phosphate synthesis, secretion, and neuroinflammation
Chung H, Ye Q, Park Y, Zuo Z, Mok J, Kanca O, Tattikota S, Lu S, Perrimon N, Lee H, Bellen H. Very-long-chain fatty acids induce glial-derived sphingosine-1-phosphate synthesis, secretion, and neuroinflammation. Cell Metabolism 2023, 35: 855-874.e5. PMID: 37084732, PMCID: PMC10160010, DOI: 10.1016/j.cmet.2023.03.022.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisAdministration of fingolimodFunctions of S1PNF-κB activationSphingosine-1-phosphate (S1P) synthesisS1P receptor antagonistsElevated VLCFAAutoimmune encephalomyelitisFatty acidsMacrophage infiltrationReceptor antagonistImmune cellsMouse modelTreatment avenuesVLCFA levelsFly gliaLong-chain fatty acidsGliaS1P pathwayS1PNeuroinflammationFingolimodVLCFAAbundant fatty acids
2022
The Role of PARP‐1 and NF‐κB in Bile‐Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells
Doukas PG, Vageli DP, Judson BL. The Role of PARP‐1 and NF‐κB in Bile‐Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells. The Laryngoscope 2022, 133: 1146-1155. PMID: 35791892, DOI: 10.1002/lary.30284.Peer-Reviewed Original ResearchConceptsHypopharyngeal cellsAcidic bileNF-κBNF-κB activationGamma-H2A histone family member XHypopharyngeal squamous cell carcinomaOncogenic profileNuclear factor kappa BPARP-1Squamous cell carcinomaB-cell lymphoma 2 expressionNF-κB transcriptional activityFactor kappa BDNA damageEnzyme-linked immunosorbent assayH2A histone family member XCell survivalDNA/RNA damageHypopharyngeal carcinogenesisReflux contentsAnti-apoptotic phenotypeCell carcinomaWidespread DNA damageBAY 11PARP-1 overexpressionPenfluridol targets acid sphingomyelinase to inhibit TNF signaling and is therapeutic against inflammatory autoimmune diseases
Chen Y, Liu R, Cui Y, Hettinghouse A, Fu W, Zhang L, Zhang C, Liu C. Penfluridol targets acid sphingomyelinase to inhibit TNF signaling and is therapeutic against inflammatory autoimmune diseases. Arthritis Research & Therapy 2022, 24: 27. PMID: 35045889, PMCID: PMC8767691, DOI: 10.1186/s13075-021-02713-6.Peer-Reviewed Original ResearchConceptsInflammatory autoimmune diseaseAnti-TNF activityNF-κB activationInflammatory arthritisAutoimmune diseasesAcid sphingomyelinase activityTherapeutic effectTumor necrosis factor αInhibitory effectTNFα-transgenic miceCollagen-induced arthritisSeverity of arthritisInflammatory cytokine productionM1 macrophage polarizationBone marrow-derived macrophagesNecrosis factor αNF-κB activitySphingomyelinase activitySmall molecule drug libraryRAW 264.7 macrophage cell lineMarrow-derived macrophagesAcid sphingomyelinaseDrug affinity responsive target stabilityCytokine productionChronic schizophrenia
2021
TNFR2/14-3-3ε signaling complex instructs macrophage plasticity in inflammation and autoimmunity
Fu W, Hu W, Yi Y, Hettinghouse A, Sun G, Bi Y, He W, Zhang L, Gao G, Liu J, Toyo-oka K, Xiao G, Solit D, Loke P, Liu C. TNFR2/14-3-3ε signaling complex instructs macrophage plasticity in inflammation and autoimmunity. Journal Of Clinical Investigation 2021, 131 PMID: 34185706, PMCID: PMC8363273, DOI: 10.1172/jci144016.Peer-Reviewed Original ResearchConceptsMacrophage polarizationMacrophage plasticityPI3K/Akt/mTORPathogenesis of inflammationMyeloid-specific deletionNF-κB activationAkt/mTORInflammatory arthritisAntiinflammatory pathwayImmunoregulatory roleAutoimmune diseasesProtective effectTherapeutic implicationsInflammationTNFR2 signalingAutoimmunityTNFR2TNFR2 activationReceptor complexDiseaseIntracellular regulatorsActivationMolecule 14TNFR1ArthritisLeucine-Rich α-2-Glycoprotein 1 Suppresses Endothelial Cell Activation Through ADAM10-Mediated Shedding of TNF-α Receptor
Pang K, Ghim M, Liu C, Tay H, Fhu C, Chia R, Qiu B, Sarathchandra P, Chester A, Yacoub M, Wilkinson F, Weston R, Warboys C, Hou H, Weinberg P, Wang X. Leucine-Rich α-2-Glycoprotein 1 Suppresses Endothelial Cell Activation Through ADAM10-Mediated Shedding of TNF-α Receptor. Frontiers In Cell And Developmental Biology 2021, 9: 706143. PMID: 34291056, PMCID: PMC8288075, DOI: 10.3389/fcell.2021.706143.Peer-Reviewed Original ResearchTumor necrosis factor receptor 1Critical limb ischemiaSera of patientsEndothelial activationEndothelial cellsLRG1 expressionElevated serum concentrationsPotential therapeutic roleLeucine-Rich αTumor necrosis factorTNF-α receptorWild-type miceEndothelial cell activationNecrosis factor receptor 1Role of LRG1NF-κB activationNF-κB signalingFactor receptor 1STNFR1 concentrationCLI patientsLimb ischemiaSerum concentrationsHealthy controlsInflammatory diseasesTherapeutic role
2020
Cell-Penetrable Peptide-Conjugated FADD Induces Apoptosis and Regulates Inflammatory Signaling in Cancer Cells
Ranjan K, Waghela BN, Vaidya FU, Pathak C. Cell-Penetrable Peptide-Conjugated FADD Induces Apoptosis and Regulates Inflammatory Signaling in Cancer Cells. International Journal Of Molecular Sciences 2020, 21: 6890. PMID: 32961826, PMCID: PMC7555701, DOI: 10.3390/ijms21186890.Peer-Reviewed Original ResearchConceptsFADD proteinCancer cellsAnti-apoptotic genesCaveolar pathwayDeath domainCellular pathwaysCancer cell proliferationCytosolic expressionFADD expressionCell deathApoptosis inducersInduces ApoptosisExpression of FasProteinCell proliferationApoptosisNF-κB activationSimultaneous regulationInflammatory signalingExpressionCellsNLRP3 inflammasome primingRegulationPathwayInflammasome primingThe temporal effects of topical NF-κB inhibition, in the in vivo prevention of bile-related oncogenic mRNA and miRNA phenotypes in murine hypopharyngeal mucosa: a preclinical model
Vageli DP, Kasle D, Doukas SG, Doukas PG, Sasaki CT. The temporal effects of topical NF-κB inhibition, in the in vivo prevention of bile-related oncogenic mRNA and miRNA phenotypes in murine hypopharyngeal mucosa: a preclinical model. Oncotarget 2020, 11: 3303-3314. PMID: 32934775, PMCID: PMC7476734, DOI: 10.18632/oncotarget.27706.Peer-Reviewed Original ResearchNF-κB inhibitorBAY 11NF-κB-related pathwaysPharmacological NF-κB inhibitorSquamous cell cancerPro-inflammatory effectsNF-κB inhibitionNF-κB activationOncogenic mRNAsAcidic bileTopical preBile refluxHypopharyngeal cancerCell cancerPreclinical modelsTopical administrationHypopharyngeal mucosaBile exposureVivo preventionTranslational explorationMiR-155MiR-21Oncogenic eventsMiRNA phenotypesPrevents overexpressionThe in vivo preventive and therapeutic properties of curcumin in bile reflux‐related oncogenesis of the hypopharynx
Doukas SG, Doukas PG, Sasaki CT, Vageli D. The in vivo preventive and therapeutic properties of curcumin in bile reflux‐related oncogenesis of the hypopharynx. Journal Of Cellular And Molecular Medicine 2020, 24: 10311-10321. PMID: 32691972, PMCID: PMC7521262, DOI: 10.1111/jcmm.15640.Peer-Reviewed Original ResearchConceptsNF-κBRecent pre-clinical studiesHuman hypopharyngeal cellsIndependent risk factorPre-clinical studiesNF-κB activationTherapeutic propertiesHypopharyngeal cellsRisk factorsMolecular eventsHypopharyngeal mucosaBile exposureImmunohistochemical analysisFuture translational developmentBile acidsOncogenic profileHypopharynxCarcinogenic effectsOncogenic functionOverexpression of RelAEpithelial cellsBileTranslational developmentExpression of genesCurcuminThe Progressive Mutagenic Effects of Acidic Bile Refluxate in Hypopharyngeal Squamous Cell Carcinogenesis: New Insights
Sasaki CT, Doukas SG, Costa J, Vageli DP. The Progressive Mutagenic Effects of Acidic Bile Refluxate in Hypopharyngeal Squamous Cell Carcinogenesis: New Insights. Cancers 2020, 12: 1064. PMID: 32344873, PMCID: PMC7281001, DOI: 10.3390/cancers12051064.Peer-Reviewed Original ResearchAcidic bileUpper aerodigestive tractAdditional risk factorsBiomarkers of progressionSquamous cell carcinogenesisNF-κB activationNeck malignanciesAerodigestive tractInvasive cancerHistopathological changesRisk factorsHypopharyngeal mucosaEarly neoplasiaMalignant lesionsP53 expressionTranslational studiesVivo modelCell carcinogenesisBileExperimental modelEarly detectionCancerNovel evidenceMutagenic effectsFirst study
2019
Dynamic Assembly of a Feedback Complex to Regulate Oncogenic B-Cell Receptor-Signaling
Lee J, Kume K, Chen Z, Xiao G, Cosgun K, Chen L, Chan L, Klemm L, Chen C, Ma N, Chan W, Forman S, Zammarchi F, Van Berkel P, Melnick A, Ngo V, Geng H, Luger S, Litzow M, McManus M, Vaidehi N, Paietta E, Meffre E, Weinstock D, Müschen M. Dynamic Assembly of a Feedback Complex to Regulate Oncogenic B-Cell Receptor-Signaling. Blood 2019, 134: 393. DOI: 10.1182/blood-2019-131270.Peer-Reviewed Original ResearchB-cell malignanciesB-cell leukemiaB cell receptorPoor clinical outcomeTransplant recipientsB cellsCytoplasmic tailClinical outcomesADC therapeuticsFatal diseaseProximity-dependent biotin identificationRefractory B-cell malignanciesPatient-derived xenograft modelsT cell growth factorNormal B cell developmentClinical outcome dataShort cytoplasmic tailHomology-directed repairB-cell receptor signalingCell membrane translocationNF-κB activationInterleukin-2 (IL-2) functionB cell developmentB-cell tumorsGenetic mouse modelsBiliary reflux as a causal factor in hypopharyngeal carcinoma: New clinical evidence and implications
Sasaki CT, Doukas SG, Costa J, Vageli DP. Biliary reflux as a causal factor in hypopharyngeal carcinoma: New clinical evidence and implications. Cancer 2019, 125: 3554-3565. PMID: 31310330, DOI: 10.1002/cncr.32369.Peer-Reviewed Original ResearchConceptsHuman hypopharyngeal squamous cell carcinomaAdjacent normal tissuesIL-6Reflux diseaseHypopharyngeal squamous cell carcinomaMiR-375Respective adjacent normal tissuesMiR-21Pilot studyEsophageal reflux diseaseIndependent risk factorNew clinical evidenceSquamous cell carcinomaOncomiR miR-21NF-κB activationMiR-21/miRTumor suppressor miR-375Quantitative polymerase chain reactionMessenger RNABiliary refluxHypopharyngeal carcinogenesisControl patientsLaryngopharyngeal refluxClinical evidenceHypopharyngeal carcinoma
2018
Galectin‐3 exacerbates ox‐LDL‐mediated endothelial injury by inducing inflammation via integrin β1‐RhoA‐JNK signaling activation
Chen X, Lin J, Hu T, Ren Z, Li L, Hameed I, Zhang X, Men C, Guo Y, Xu D, Zhan Y. Galectin‐3 exacerbates ox‐LDL‐mediated endothelial injury by inducing inflammation via integrin β1‐RhoA‐JNK signaling activation. Journal Of Cellular Physiology 2018, 234: 10990-11000. PMID: 30536538, PMCID: PMC6590151, DOI: 10.1002/jcp.27910.Peer-Reviewed Original ResearchMeSH KeywordsAtherosclerosisCell Adhesion MoleculesCell SurvivalEndothelium, Vascularfas ReceptorGalectin 3Gene Expression RegulationHuman Umbilical Vein Endothelial CellsHumansInflammationIntegrin beta1JNK Mitogen-Activated Protein KinasesLipoproteins, LDLMAP Kinase Signaling SystemrhoA GTP-Binding ProteinConceptsHuman umbilical vascular endothelial cellsEndothelial injuryGal-3P-JNKInflammatory factorsGTP-RhoAGalectin-3Plasma galectin-3Systemic inflammatory disorderEndothelial cell injuryPathogenesis of atherosclerosisLow-density lipoproteinNF-κB activationVascular endothelial cellsEndothelial dysfunctionP-IKKβAS patientsInflammatory disordersP-p65P-IKKαCardiovascular diseaseOx-LDLCell injuryCCK8 assayControl groupA Phase II Trial of Bortezomib and Vorinostat in Mantle Cell Lymphoma and Diffuse Large B-cell Lymphoma
Yazbeck V, Shafer D, Perkins EB, Coppola D, Sokol L, Richards KL, Shea T, Ruan J, Parekh S, Strair R, Flowers C, Morgan D, Kmieciak M, Bose P, Kimball A, Badros AZ, Baz R, Lin HY, Zhao X, Reich RR, Tombes MB, Shrader E, Sankala H, Roberts JD, Sullivan D, Grant S, Holkova B. A Phase II Trial of Bortezomib and Vorinostat in Mantle Cell Lymphoma and Diffuse Large B-cell Lymphoma. Clinical Lymphoma Myeloma & Leukemia 2018, 18: 569-575.e1. PMID: 30122201, PMCID: PMC11673799, DOI: 10.1016/j.clml.2018.05.023.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic Combined Chemotherapy ProtocolsBortezomibDrug Resistance, NeoplasmFemaleFollow-Up StudiesHumansLymphoma, Large B-Cell, DiffuseLymphoma, Mantle-CellMaleMiddle AgedNeoplasm Recurrence, LocalPrognosisProspective StudiesSalvage TherapySurvival RateVorinostatConceptsLarge B-cell lymphomaPhase II trialStable diseaseProgressive diseaseB-cell lymphomaPartial responseII trialCohort BCohort ADay 1Median progression-free survivalNonrandomized phase II trialDiffuse large B-cell lymphomaProgression-free survivalHistone deacetylase inhibitor vorinostatOverall response rateCombination of bortezomibMantle cell lymphomaNF-κB activationProteasome inhibitor bortezomibCell lymphoma cellsPresent multicenterRefractory MCLClinical responseCohort CSIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65
Li P, Jin Y, Qi F, Wu F, Luo S, Cheng Y, Montgomery RR, Qian F. SIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65. Frontiers In Cellular And Infection Microbiology 2018, 8: 113. PMID: 29686974, PMCID: PMC5900784, DOI: 10.3389/fcimb.2018.00113.Peer-Reviewed Original ResearchConceptsToll-like receptor 3Dengue virusInflammatory responseDENV infectionDengue disease severityNF-κB p65Innate immune responseNF-κB activationDomain of p65Overexpression of SIRT6Chemokine productionProinflammatory cytokinesDengue patientsInflammatory cytokinesP65 functionImmune responseLike receptorsDisease severityNegative regulatorReceptor 3Variable severityP65SIRT6CytokinesVirusInhibiting Integrin α5 Cytoplasmic Domain Signaling Reduces Atherosclerosis and Promotes Arteriogenesis
Budatha M, Zhang J, Zhuang ZW, Yun S, Dahlman JE, Anderson DG, Schwartz MA. Inhibiting Integrin α5 Cytoplasmic Domain Signaling Reduces Atherosclerosis and Promotes Arteriogenesis. Journal Of The American Heart Association 2018, 7: e007501. PMID: 29382667, PMCID: PMC5850249, DOI: 10.1161/jaha.117.007501.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic DiseasesAtherosclerosisCyclic Nucleotide Phosphodiesterases, Type 4Disease Models, AnimalExtracellular MatrixFibronectinsFibrosisGenetic Predisposition to DiseaseHindlimbInflammation MediatorsIntegrin alpha2Integrin alpha5IschemiaLeukocytesMaleMatrix MetalloproteinasesMice, Inbred C57BLMice, Knockout, ApoEMuscle, SkeletalNeovascularization, PhysiologicNF-kappa BPhenotypePlaque, AtheroscleroticSignal TransductionVascular RemodelingConceptsEndothelial inflammatory activationAtherosclerotic plaque sizeInflammatory activationPlaque stabilityVascular remodelingEndothelial NF-κB activationSmooth muscle cell contentPlaque sizeFemoral artery ligationMuscle cell contentTreatment of atherosclerosisInflammatory gene expressionPotential therapeutic targetFibrous cap thicknessNF-κB activationSmaller atherosclerotic plaquesArtery ligationAortic rootHindlimb ischemiaCompensatory remodelingAtherosclerotic plaquesTherapeutic targetLeukocyte contentMetalloproteinase expressionEndothelial basement membraneNF-κB-Chromatin Interactions Drive Diverse Phenotypes by Modulating Transcriptional Noise
Wong VC, Bass VL, Bullock ME, Chavali AK, Lee REC, Mothes W, Gaudet S, Miller-Jensen K. NF-κB-Chromatin Interactions Drive Diverse Phenotypes by Modulating Transcriptional Noise. Cell Reports 2018, 22: 585-599. PMID: 29346759, PMCID: PMC5812697, DOI: 10.1016/j.celrep.2017.12.080.Peer-Reviewed Original ResearchConceptsTranscriptional noiseIntegration sitesDiverse phenotypesRNA polymerase II regulationNoisy gene expressionGenomic integration sitesLive-cell imagingNF-κB activationChromatin environmentChromatin stateViral activationChromatin interactionsTranscript abundanceTranscription factor nuclear factor κBDivergent phenotypesGene expressionNoisy expressionNF-κBTranscript numbersNuclear factor κBPhenotypeTumor necrosis factorFactor κBActivationExpression
2017
An inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes
Yan J, Hedl M, Abraham C. An inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes. Journal Of Clinical Investigation 2017, 127: 2192-2205. PMID: 28436939, PMCID: PMC5451247, DOI: 10.1172/jci86282.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusCarrier ProteinsCase-Control StudiesCytokinesEnterococcus faecalisGene ExpressionGenetic Association StudiesGenetic Predisposition to DiseaseHEK293 CellsHeterozygoteHumansInflammatory Bowel DiseasesMacrophagesMAP Kinase Signaling SystemMyeloid CellsPolymorphism, Single NucleotidePrimary Cell CultureReceptors, Pattern RecognitionRisk FactorsStaphylococcus aureusConceptsInflammatory bowel diseasePattern recognition receptor signalingDisease risk variantsIntestinal immune homeostasisActivation of MAPKIBD risk lociINAVAPrimary human cellsBacterial clearanceIntestinal myeloid cellsRisk lociAutophagy pathwayProper regulationIntronic regionsHuman cellsImmune homeostasisReceptor signalingDownstream signalsPRR stimulationReactive oxygenIntestinal microbesNF-κB activationGenesNF-κB pathwayMAPK
2016
Myelin phagocytosis by astrocytes after myelin damage promotes lesion pathology
Ponath G, Ramanan S, Mubarak M, Housley W, Lee S, Sahinkaya FR, Vortmeyer A, Raine CS, Pitt D. Myelin phagocytosis by astrocytes after myelin damage promotes lesion pathology. Brain 2016, 140: 399-413. PMID: 28007993, PMCID: PMC5841057, DOI: 10.1093/brain/aww298.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsAnimals, NewbornAstrocytesCell ProliferationCells, CulturedChild, PreschoolCultureCytokinesDemyelinating Autoimmune Diseases, CNSEndocytosisFemaleHumansHydrazonesMacrophagesMaleMiddle AgedMyelin SheathPhagocytosisRatsRats, Sprague-DawleyStrokeTime FactorsTransforming Growth Factor betaConceptsMyelin injuryMyelin phagocytosisMyelin debrisMultiple sclerosis lesionsMultiple sclerosisLesion pathologySclerosis lesionsAcute multiple sclerosis lesionsCentral nervous system pathologyProgressive multifocal leukoencephalopathyNervous system pathologySecretion of chemokinesNF-κB activationElevated chemokine expressionHypertrophic astrocytesMost astrocytesMyelin uptakeMultifocal leukoencephalopathyFirst-line responseAcute lesionsMyelin damageReactive astrocytesChemokine expressionAstroglial responseImmune cellsUnidirectional and sustained delivery of the proresolving lipid mediator resolvin D1 from a biodegradable thin film device
Lance KD, Chatterjee A, Wu B, Mottola G, Nuhn H, Lee PP, Sansbury BE, Spite M, Desai TA, Conte MS. Unidirectional and sustained delivery of the proresolving lipid mediator resolvin D1 from a biodegradable thin film device. Journal Of Biomedical Materials Research Part A 2016, 105: 31-41. PMID: 27508346, PMCID: PMC5124518, DOI: 10.1002/jbm.a.35861.Peer-Reviewed Original ResearchConceptsResolvin D1Rat carotid artery modelProresolving lipid mediatorsHuman vascular endothelialNF-κB activationSmooth muscle cellsCarotid artery modelTissue injuryEvidence of cytotoxicityRvD1Lipid mediatorsRabbit aortaVSMC migrationMuscle cellsFlow chamber systemBlood vesselsLocal deliveryVascular endothelialArtery modelRelevant levelsVivoTissueD1Vascular tissueDaysFADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis
Ranjan K, Pathak C. FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis. Scientific Reports 2016, 6: 22787. PMID: 26972597, PMCID: PMC4789601, DOI: 10.1038/srep22787.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell LineCell SurvivalFas-Associated Death Domain ProteinHCT116 CellsHEK293 CellsHeLa CellsHT29 CellsHumansInhibitor of Apoptosis ProteinsMCF-7 CellsMiceNF-kappa BNIH 3T3 CellsProtein BindingRepressor ProteinsRNA InterferenceTumor Necrosis Factor-alphaUbiquitin-Protein LigasesUbiquitinationConceptsCell deathProcaspase-8Molecular mechanismsCellular FLICE-like inhibitory proteinFLICE-like inhibitory proteinExpression of cFLIPLCell death signalingApoptosis protein 2Apoptotic cell death signalingHEK 293T cellsNovel molecular mechanismApoptotic cell deathNF-κB activationFasL stimulationCellular inhibitorE3 ubiquitinTNF-α stimulationDeath domainDeath inducingDeath signalingEctopic expressionFADDCaspase-8NF-κBCell survival
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