2025
Meningeal lymphatics-microglia axis regulates synaptic physiology
Kim K, Abramishvili D, Du S, Papadopoulos Z, Cao J, Herz J, Smirnov I, Thomas J, Colonna M, Kipnis J. Meningeal lymphatics-microglia axis regulates synaptic physiology. Cell 2025, 188: 2705-2719.e23. PMID: 40120575, PMCID: PMC12086007, DOI: 10.1016/j.cell.2025.02.022.Peer-Reviewed Original ResearchConceptsBehavioral alterationsAging-associated cognitive declineMemory taskNeural mechanismsIL-6Cognitive declineIL-6-dependent mechanismInhibitory synaptic inputsCortical circuitryBehavioral changesMeningeal lymphaticsInterleukin-6 geneIL-6 signalingAge-associatedSynaptic inputsLymphatic dysfunctionLymphatic functionCerebrospinal fluidProlonged impairmentIncreased expressionNeurodegenerative conditionsLymphaticsPotential targetDysfunctionDeficitsTracing the origins of fibrotic fibroblasts: does the name matter? Look at the genes!
Mailleux A, Justet A. Tracing the origins of fibrotic fibroblasts: does the name matter? Look at the genes! European Respiratory Journal 2025, 65: 2402170. PMID: 39915043, DOI: 10.1183/13993003.02170-2024.Peer-Reviewed Original ResearchGrover disease shows type 2 immune activation and improves with dupilumab
Murphy M, Junejo M, Rufin O, Cohen J, Nelson C, Damsky W. Grover disease shows type 2 immune activation and improves with dupilumab. British Journal Of Dermatology 2025, 192: 939-941. PMID: 39775460, DOI: 10.1093/bjd/ljaf005.Peer-Reviewed Original Research
2024
Heterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption
Ren P, Jiang B, Hassab A, Li G, Li W, Assi R, Tellides G. Heterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption. Arteriosclerosis Thrombosis And Vascular Biology 2024, 45: 260-276. PMID: 39697172, PMCID: PMC12053597, DOI: 10.1161/atvbaha.124.321706.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic AneurysmCell LineageDisease Models, AnimalGene Expression ProfilingHomeobox Protein Nkx-2.5HumansMaleMarfan SyndromeMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleMyosin Heavy ChainsNeural CrestPhenotypeReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionSingle-Cell AnalysisTranscription, GeneticTranscriptomeTransforming Growth Factor betaWnt1 ProteinConceptsSmooth muscle cell clustersSmooth muscle cellsAortic smooth muscle cellsNeural crest-derived smooth muscle cellsCardiac derivativesMurine aortic smooth muscle cellsNeural crest originReceptor deletionAortic rootAdult miceNeural crest progenitorsNKX2-5Proximal aortaTranscriptional changesMouse modelTGFB signalingMuscle cellsConditional deletionAdult human aortaEmbryological originIncreased expressionAnalyzed single-cell transcriptomesTGFB receptorsBasal stateAortic homeostasisThe Role of NOXA in Venetoclax Treatment Response in Multiple Myeloma
Shivaram S, Yan H, Tang H, Anderson H, Kaddoura M, Wiedmeier-Nutor J, Tian S, Howe M, Bolarinwa A, Zepeda Mendoza C, Gupta V, Lehman S, Mitsiades C, Bergsagel P, Braggio E, Boise L, Fonseca R, Maura F, Kumar S, Baughn L. The Role of NOXA in Venetoclax Treatment Response in Multiple Myeloma. Blood 2024, 144: 4635-4635. DOI: 10.1182/blood-2024-205385.Peer-Reviewed Original ResearchMayo Clinic cohortNoxa proteinMultiple myelomaG alleleIncreased expressionGene expressionCyclin D1Clinical cohortExpression of CCND1Cell linesAllele specific effectsBCL-2 inhibitor venetoclaxLevels of NoxaHistone mark H3K27acG risk allelePrimary cytogenetic abnormalityPlasma cell malignancyAssociated with increased expressionRNA sequencing dataHuman myeloma cell linesKO cell linesWestern blottingAnalyzed whole-exomeChIP-seqWhole genomeDexamethasone Targets E2F4 to Induce Erythroid Progenitor Renewal
Papoin J, Schulz V, Khan F, Barnes B, Lipton J, Steiner L, Narla M, Gallagher P, Blanc L. Dexamethasone Targets E2F4 to Induce Erythroid Progenitor Renewal. Blood 2024, 144: 1076. DOI: 10.1182/blood-2024-211687.Peer-Reviewed Original ResearchDiamond-Blackfan anemiaCD34+ cellsErythroid progenitorsSteroid responsivenessExpression of E2F4Peripheral bloodBone marrowE2F4 expressionDEX treatmentCultured CD34+ cellsInherited bone marrow failure syndromeMechanisms of steroid responseSide effectsBone marrow failure syndromesDiamond-Blackfan anemia patientsBone marrow erythroid progenitorsIncreased expressionMechanisms of corticosteroid actionAssociated with side effectsIncreased risk of infectionMarrow failure syndromesResponse to steroidsGene promoterSerum-free culture systemMarrow erythroid progenitorsMolecular Profiling of Mouse Models of Loss or Gain of Function of the KCNT1 (Slack) Potassium Channel and Antisense Oligonucleotide Treatment
Sun F, Wang H, Wu J, Quraishi I, Zhang Y, Pedram M, Gao B, Jonas E, Nguyen V, Wu S, Mabrouk O, Jafar-nejad P, Kaczmarek L. Molecular Profiling of Mouse Models of Loss or Gain of Function of the KCNT1 (Slack) Potassium Channel and Antisense Oligonucleotide Treatment. Biomolecules 2024, 14: 1397. PMID: 39595574, PMCID: PMC11591899, DOI: 10.3390/biom14111397.Peer-Reviewed Original ResearchWild-type miceKO miceSpectrum of epilepsy syndromesAntisense oligonucleotidesGain-of-function variantsAntisense oligonucleotide treatmentEpileptic phenotypePotassium channelsKCNT1Molecular profilingOligonucleotide treatmentAnimal modelsEpilepsy syndromesC-terminal mutationsIncreased expressionCerebral cortexMiceExpression of multiple proteinsComprehensive proteomic analysisDisease modelsCortical mitochondriaMolecular differencesDensity of mitochondrial cristaeMitochondrial membraneTreatmentCell-specific cross-talk proteomics reveals cathepsin B signaling as a driver of glioblastoma malignancy near the subventricular zone
Norton E, Whaley L, Jones V, Brooks M, Russo M, Morderer D, Jessen E, Schiapparelli P, Ramos-Fresnedo A, Zarco N, Carrano A, Rossoll W, Asmann Y, Lam T, Chaichana K, Anastasiadis P, Quiñones-Hinojosa A, Guerrero-Cázares H. Cell-specific cross-talk proteomics reveals cathepsin B signaling as a driver of glioblastoma malignancy near the subventricular zone. Science Advances 2024, 10: eadn1607. PMID: 39110807, PMCID: PMC11305394, DOI: 10.1126/sciadv.adn1607.Peer-Reviewed Original ResearchConceptsBrain tumor-initiating cellsLateral ventricleNeuronal maturationMalignancy-associated phenotypesSubventricular zone contactIncreased expression of cathepsin BMalignant primary brain tumorTumor-initiating cellsAggressive malignant primary brain tumorPrimary brain tumorTumor microenvironment researchExpression of cathepsin BNeural stem/progenitor cellsCathepsin BInduction of senescenceStem/progenitor cellsCell-intrinsicSubventricular zoneCross-talkTherapeutic strategiesBrain tumorsIncreased expressionGBM biologyLentiviral knockdownGlioblastomaFatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring
Sun J, Esplugues E, Bort A, Cardelo M, Ruz-Maldonado I, Fernández-Tussy P, Wong C, Wang H, Ojima I, Kaczocha M, Perry R, Suárez Y, Fernández-Hernando C. Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring. Nature Metabolism 2024, 6: 741-763. PMID: 38664583, PMCID: PMC12355809, DOI: 10.1038/s42255-024-01019-6.Peer-Reviewed Original ResearchConceptsFatty acid binding protein 5Tumor-associated macrophagesHepatocellular carcinomaImmunosuppressive phenotype of tumor-associated macrophagesIncreased CD8+ T cell activationCD8+ T cell activationPhenotype of tumor-associated macrophagesPro-inflammatory tumor microenvironmentCo-stimulatory molecules CD80T cell activationHepatocellular carcinoma burdenTransformation of hepatocytesBinding protein 5Potential therapeutic approachImmunosuppressive phenotypeTumor microenvironmentFerroptosis-induced cell deathMale miceEnhanced ferroptosisTherapeutic approachesPharmacological inhibitionGenetic ablationIncreased expressionSingle-cell atlasAnalysis of transformed cellsGenetic contribution to microglial activation in schizophrenia
Koskuvi M, Pörsti E, Hewitt T, Räsänen N, Wu Y, Trontti K, McQuade A, Kalyanaraman S, Ojansuu I, Vaurio O, Cannon T, Lönnqvist J, Therman S, Suvisaari J, Kaprio J, Blurton-Jones M, Hovatta I, Lähteenvuo M, Rolova T, Lehtonen Š, Tiihonen J, Koistinaho J. Genetic contribution to microglial activation in schizophrenia. Molecular Psychiatry 2024, 29: 2622-2633. PMID: 38519640, PMCID: PMC11420079, DOI: 10.1038/s41380-024-02529-1.Peer-Reviewed Original ResearchIngenuity Pathway AnalysisGene OntologyMajor histocompatibility complexAffected twinHuman induced pluripotent stem cell-derived microgliaExtracellular matrix signalingUpregulation of major histocompatibility complexHealthy individualsIncreased expression of inflammatory genesIncreased expressionMicroglial activationResponse to clozapineStem cell-derived microgliaBrain-resident immune cellsResponse to interleukin-1 betaPathophysiology of schizophreniaInvolvement of neuroinflammatory processesResident immune cellsExpression of inflammatory genesIncreased microglial activationInterleukin-1 betaAberrant activation of microgliaHuman cell modelsRNA sequencingInvading pathogensSulfide quinone oxidoreductase contributes to voltage sensing of the mitochondrial permeability transition pore
Griffiths K, Wang A, Jonas E, Levy R. Sulfide quinone oxidoreductase contributes to voltage sensing of the mitochondrial permeability transition pore. The FASEB Journal 2024, 38: e23494. PMID: 38376922, PMCID: PMC11082757, DOI: 10.1096/fj.202301280r.Peer-Reviewed Original ResearchConceptsMitochondrial permeability transition poreSulfide quinone oxidoreductasePermeability transition poreTransition poreFragile X syndromeQuinone oxidoreductaseMouse heart mitochondriaHeart mitochondriaGenetic silencingAlzheimer's diseaseCardiac mitochondriaPharmacological inhibitionMitochondriaOpen probabilityOxidoreductaseX syndromeTherapeutic targetIncreased expressionModel systemLack of translationVoltage-gated channelsIsolated-perfused heartsPathological openingMyocardial ischemiaClinical therapy
2023
Final 36-Month Outcomes from the Multicenter DynamX Study Evaluating a Novel Thin-Strut Novolimus-Eluting Coronary Bioadaptor System and Supporting Preclinical Data
Verheye S, Vrolix M, Montorfano M, Giannini F, Bedogni F, Dubois C, De Bruyne B, Costa R, Chamié D, Costa J, Abizaid A, Colombo A. Final 36-Month Outcomes from the Multicenter DynamX Study Evaluating a Novel Thin-Strut Novolimus-Eluting Coronary Bioadaptor System and Supporting Preclinical Data. Reviews In Cardiovascular Medicine 2023, 24: 221. PMID: 39076703, PMCID: PMC11266769, DOI: 10.31083/j.rcm2408221.Peer-Reviewed Original ResearchDrug-eluting stentsOptical coherence tomographyTarget lesion revascularizationExpression of contractile genesPreclinical studiesLesion revascularizationGene expression profilesClinically-driven target lesion revascularizationIntention-to-treat populationContractile genesCoronary arteryIncreased expressionLong-term adverse outcomesClinical follow-upLate lumen enlargementCell gene expression profilesRestoring vessel functionTarget vessel revascularizationTarget lesion failureReal-time polymerase chain reactionPreclinical dataExpression profilesClinical outcomesLumen enlargementCardiac deathHERV1-env Induces Unfolded Protein Response Activation in Autoimmune Liver Disease: A Potential Mechanism for Regulatory T Cell Dysfunction.
Subramanian K, Paul S, Libby A, Patterson J, Arterbery A, Knight J, Castaldi C, Wang G, Avitzur Y, Martinez M, Lobritto S, Deng Y, Geliang G, Kroemer A, Fishbein T, Mason A, Dominguez-Villar M, Mariappan M, Ekong U. HERV1-env Induces Unfolded Protein Response Activation in Autoimmune Liver Disease: A Potential Mechanism for Regulatory T Cell Dysfunction. The Journal Of Immunology 2023, 210: 732-744. PMID: 36722941, PMCID: PMC10691554, DOI: 10.4049/jimmunol.2100186.Peer-Reviewed Original ResearchConceptsAutoimmune hepatitisDe novo autoimmune hepatitisRegulatory T cell dysfunctionUnfolded protein responseNovo autoimmune hepatitisTregs of patientsAutoimmune liver diseaseIL-17A productionRegulatory T cellsT cell dysfunctionTreg suppressive functionExpression of RORCER stressEndoplasmic reticulum stressTreg plasticityLiver diseaseCell dysfunctionProtein response activationT cellsUnfolded protein response activationSuppressive functionIncreased expressionEffector propertiesReticulum stressPotential mechanisms
2022
Transcriptomic profiling identifies genomic markers associated with benefit from stereotactic body radiation therapy (SBRT) in oligoprogressive metastatic renal cell carcinoma (mRCC).
Zengin Z, Govindarajan A, Muddasani R, Salgia N, Sayegh N, Tripathi N, Salgia S, Meza L, Zhang J, Chawla N, Chehrazi-Raffle A, Malhotra J, Dizman N, Hsu J, Castro D, Byron S, Dandapani S, Pal S. Transcriptomic profiling identifies genomic markers associated with benefit from stereotactic body radiation therapy (SBRT) in oligoprogressive metastatic renal cell carcinoma (mRCC). Journal Of Clinical Oncology 2022, 40: 4555-4555. DOI: 10.1200/jco.2022.40.16_suppl.4555.Peer-Reviewed Original ResearchMetastatic renal cell carcinomaStereotactic body radiation therapySystemic treatmentSystemic therapyLess benefitCompletion of SBRTRole of SBRTHigh expressionBody radiation therapyRenal cell carcinomaT-testStudent's t-testHypoxia-related genesCommon histologyOligoprogressive diseaseClinicopathologic characteristicsMedian ageFischer's exactClinical benefitCell carcinomaClear cellsRadiation therapyTreatment durationTreatment changesIncreased expression
2021
Paclitaxel increases axonal localization and vesicular trafficking of Nav1.7
Akin EJ, Alsaloum M, Higerd GP, Liu S, Zhao P, Dib-Hajj FB, Waxman SG, Dib-Hajj SD. Paclitaxel increases axonal localization and vesicular trafficking of Nav1.7. Brain 2021, 144: 1727-1737. PMID: 33734317, PMCID: PMC8320304, DOI: 10.1093/brain/awab113.Peer-Reviewed Original ResearchConceptsDorsal root ganglion neuronsChemotherapy-induced peripheral neuropathyGanglion neuronsSensory axonsNav1.7 channelsPTX treatmentSensory neuronsHuman sensory neuronsEffect of paclitaxelSodium channel Nav1.7Chemotherapy drug paclitaxelAxonal vesicular transportConcentrations of paclitaxelNav1.7 mRNAInflammatory mediatorsNav1.7 expressionPeripheral neuropathyInflammatory milieuPrimary afferentsInflammatory conditionsChannel expressionChannel Nav1.7Nav1.7Increased expressionAxonal localizationNicotinic regulation of local and long-range input balance drives top-down attentional circuit maturation
Falk E, Norman K, Garkun Y, Demars M, Im S, Taccheri G, Short J, Caro K, McCraney S, Cho C, Smith M, Lin H, Koike H, Bateh J, Maccario P, Waltrip L, Janis M, Morishita H. Nicotinic regulation of local and long-range input balance drives top-down attentional circuit maturation. Science Advances 2021, 7: eabe1527. PMID: 33674307, PMCID: PMC7935362, DOI: 10.1126/sciadv.abe1527.Peer-Reviewed Original ResearchConceptsFrontal neuronsModel of fragile X syndromeMouse model of fragile X syndromeNicotinic cholinergic systemTop-down neuronsTreating cognitive deficitsBehavior in adulthoodNicotinic signalingCircuit maturationFragile X syndromeNicotine regulationCholinergic inputMouse modelIncreased expressionCognitive deficitsCortex developmentCholinergic systemCognitive functionTop-down projectionsX syndromeNeurodevelopmental disordersNeuronsVisual cortexAdolescentsMaturation process
2020
An omic approach to congenital diaphragmatic hernia: a pilot study of genomic, microRNA, and metabolomic profiling
Piersigilli F, Syed M, Lam TT, Dotta A, Massoud M, Vernocchi P, Quagliariello A, Putignani L, Auriti C, Salvatori G, Bagolan P, Bhandari V. An omic approach to congenital diaphragmatic hernia: a pilot study of genomic, microRNA, and metabolomic profiling. Journal Of Perinatology 2020, 40: 952-961. PMID: 32080334, DOI: 10.1038/s41372-020-0623-3.Peer-Reviewed Original ResearchConceptsCongenital diaphragmatic herniaCDH patientsTracheal aspiratesDiaphragmatic herniaAge-matched control patientsAge-matched controlsChromosomal microarray analysisControl patientsControl neonatesBlood samplesPatientsMiR expressionIncreased expressionPilot studyMiR-19bMiR-18MiR-20aMiR-16Genetic mutationsMetabolomic profilingHerniaMiR-17NeonatesMicroarray analysisMetabolic fingerprints
2019
Evaluation of miR-135a/b expression in endometriosis lesions
Petracco R, De Oliveira Dias A, Taylor H, Petracco Á, Badalotti M, Da Rosa Michelon J, Marinowic DR, Hentschke M, De Azevedo P, Zanirati G, Machado DC. Evaluation of miR-135a/b expression in endometriosis lesions. Biomedical Reports 2019, 11: 181-187. PMID: 31565224, PMCID: PMC6759580, DOI: 10.3892/br.2019.1237.Peer-Reviewed Original ResearchEndometriosis lesionsEndometrium tissuesSecretory phaseProliferative phaseExpression levelsReverse transcription‑quantitative polymerase chain reaction assaysEctopic endometriosis lesionsTranscription-quantitative polymerase chain reaction assaysPathogenesis of endometriosisEctopic endometrium tissuesEutopic endometrium tissuesPolymerase chain reaction assaysEndometrial functioningEndometrial receptivityMenstrual cycleChain reaction assaysLaparoscopic surgeryPost-transcriptional regulationEmbryo implantationQuantitative polymerase chain reaction assaysShort noncoding RNAsB expressionIncreased expressionExpression of genesLesions
2017
Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12
Tan J, Tedrow JR, Nouraie M, Dutta JA, Miller DT, Li X, Yu S, Chu Y, Juan-Guardela B, Kaminski N, Ramani K, Biswas PS, Zhang Y, Kass DJ. Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12. The Journal Of Immunology 2017, 198: 2269-2285. PMID: 28179498, PMCID: PMC5337810, DOI: 10.4049/jimmunol.1600610.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsLung injuryPulmonary fibrosisT cellsFibrotic lung injuryIPF lung fibroblastsExperimental lung injuryT-cell pathwayApoptosis-resistant fibroblastsMatrix-producing cellsChemoattractant CXCL12Exaggerated fibrosisIPF phenotypeCollagen-producing cellsTranscription factor Twist1Prosurvival phenotypeFibrosisTwist1 expressionIncreased expressionLung fibroblastsCXCL12Low expressionHigh expressionCell pathwaysSOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer
Mu P, Zhang Z, Benelli M, Karthaus W, Hoover E, Chen C, Wongvipat J, Ku S, Gao D, Cao Z, Shah N, Adams E, Abida W, Watson P, Prandi D, Huang C, de Stanchina E, Lowe S, Ellis L, Beltran H, Rubin M, Goodrich D, Demichelis F, Sawyers C. SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer. Science 2017, 355: 84-88. PMID: 28059768, PMCID: PMC5247742, DOI: 10.1126/science.aah4307.Peer-Reviewed Original ResearchConceptsLineage plasticityRB1 functionHuman prostate cancer modelProstate cancer modelLoss of TP53Basal-like cellsTumor suppressor geneTranscription factor Sox2Antiandrogen therapyProstate cancerInhibiting Sox2 expressionLineage switchAntiandrogen resistanceCancer modelsTumor cellsSuppressor geneSOX2 expressionIncreased expressionTP53TumorCell lineagesCellular plasticityIn vitroPhenotypic shiftCancer
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