2025
Type I interferons induce guanylate-binding proteins and lysosomal defense in hepatocytes to control malaria
Marques-da-Silva C, Schmidt-Silva C, Bowers C, Charles-Chess N, Samuel C, Shiau J, Park E, Yuan Z, Kim B, Kyle D, Harty J, MacMicking J, Kurup S. Type I interferons induce guanylate-binding proteins and lysosomal defense in hepatocytes to control malaria. Cell Host & Microbe 2025, 33: 529-544.e9. PMID: 40168996, DOI: 10.1016/j.chom.2025.03.008.Peer-Reviewed Original ResearchConceptsGuanylate-binding proteinsType I interferonPlasmodium infectionI interferonParasitophorous vacuoleLiver-stage malariaNon-immune cellsInfected host cellsCaspase-1 inflammasomeNADPH oxidase 2Clinical malariaControl malariaLysosomal fusionAntimicrobial programPlasmodium parasitesHost cellsInfected erythrocytesProtective immunityMalariaPlasmodiumGenetic inhibitionCaspase-1Immunization programsImmune circuitsMouse hepatocytes
2024
Loss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis
Dave J, Chakraborty R, Agyemang A, Ntokou A, Saito J, Ballabh P, Martin K, Greif D. Loss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis. Stroke 2024, 55: 2340-2352. PMID: 39129597, PMCID: PMC11347087, DOI: 10.1161/strokeaha.123.045248.Peer-Reviewed Original ResearchAngiopoietin-2Germinal matrix hemorrhage-intraventricular hemorrhagePerinatal lethalityEndothelial cell hyperproliferationEndothelial cellsBrain pericytesGenetic inhibitionVascular cellsBlood-brain barrier integrityBlood-brain barrier developmentBrain vascular cellsAbnormal vessel morphologyVessel morphologyProlonged survivalRegulating cross-talkMutant endothelial cellsHuman brain pericytesGerminal matrixCell hyperproliferationPhosphorylates Tie2Embryonic miceCellular sourceBarrier integrityGenetic ablationTherapeutic effectGlycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis
Khanal S, Liu Y, Bamidele A, Wixom A, Washington A, Jalan-Sakrikar N, Cooper S, Vuckovic I, Zhang S, Zhong J, Johnson K, Charlesworth M, Kim I, Yeon Y, Yoon S, Noh Y, Meroueh C, Timbilla A, Yaqoob U, Gao J, Kim Y, Lucien F, Huebert R, Hay N, Simons M, Shah V, Kostallari E. Glycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis. Science Advances 2024, 10: eadn5228. PMID: 38941469, PMCID: PMC11212729, DOI: 10.1126/sciadv.adn5228.Peer-Reviewed Original ResearchConceptsHepatic stellate cellsLiver fibrosisExtracellular vesiclesEV releaseHistone 3 lysine 9 acetylationExtracellular vesicle releaseIncreased EV releaseFibrotic gene expressionNanosized extracellular vesiclesPromoter regionVesicle releasePotential therapeutic targetGene expressionGenetic inhibitionSpatial transcriptomicsStellate cellsGlycolysisUp-regulatedFibrosisTherapeutic targetPericentral zoneLiverPathwayAmplificationExpression
2023
Effect Of Comt Genetic Background And Stress On Pain Following Tibial Fracture
Chen J, Wu Y, Wang Y, Sandu C, Gu E, Jordt S, Terrando N, Nackley A. Effect Of Comt Genetic Background And Stress On Pain Following Tibial Fracture. Journal Of Pain 2023, 24: 30. DOI: 10.1016/j.jpain.2023.02.098.Peer-Reviewed Original ResearchDepressive-like behaviorStress fracture groupTail suspension testTibial fracturesSham stressAbdominal sitesSuspension testSham–sham groupVon Frey filamentsWild-type miceAbdominal hyperalgesiaMechanical hyperalgesiaMechanical hypersensitivityImmobility timeWT miceBody painType miceHyperalgesiaPainSpinal needleActivity genotypeMonth time periodGenetic inhibitionStress groupCOMT genotype
2018
Cyclophilin D-Dependent Mitochondrial Proton Leak in ß Cells Promotes Basal Insulin Secretion
ALSABEEH N, TADDEO E, WIKSTRÖM J, RITOU E, STILES L, KIBBEY R, LIESA M, SHIRIHAI O. Cyclophilin D-Dependent Mitochondrial Proton Leak in ß Cells Promotes Basal Insulin Secretion. Diabetes 2018, 67 DOI: 10.2337/db18-312-lb.Peer-Reviewed Original ResearchMitochondrial proton leakProton leakPermeability transition poreInhibition of CypDBasal hypersecretionCyclophilin DMolecular mechanismsInsulin secretionTransition poreGenetic inhibitionHigh-fat diet animalsAmino acidsDevelopment of diabetesHypersecretion of insulinNovel targetBeta-cell failureBasal insulin secretionBasal hyperinsulinemiaFatty acidsPrediabetic subjectsPrediabetic animalsLow conductance stateBlood glucoseBasal secretionPharmacological stimulationProduction of BMP4 by endothelial cells is crucial for endogenous thymic regeneration
Wertheimer T, Velardi E, Tsai J, Cooper K, Xiao S, Kloss CC, Ottmüller KJ, Mokhtari Z, Brede C, deRoos P, Kinsella S, Palikuqi B, Ginsberg M, Young LF, Kreines F, Lieberman SR, Lazrak A, Guo P, Malard F, Smith OM, Shono Y, Jenq RR, Hanash AM, Nolan DJ, Butler JM, Beilhack A, Manley NR, Rafii S, Dudakov JA, van den Brink MRM. Production of BMP4 by endothelial cells is crucial for endogenous thymic regeneration. Science Immunology 2018, 3 PMID: 29330161, PMCID: PMC5795617, DOI: 10.1126/sciimmunol.aal2736.Peer-Reviewed Original ResearchConceptsKey transcription factorEndothelial cellsEndogenous tissue regenerationThymic epithelial cellsTranscription factorsBMP4 pathwayThymic endothelial cellsDownstream targetsBMP4Genetic inhibitionThymocyte developmentTEC developmentEpithelial cellsKey mediatorEndogenous regenerationRemarkable abilityCritical pathwaysTissue regenerationPathwayCellsRegenerationEndogenous thymic regenerationT cell immunityPotential clinical approachThymic damage
2011
Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase
Alavian KN, Li H, Collis L, Bonanni L, Zeng L, Sacchetti S, Lazrove E, Nabili P, Flaherty B, Graham M, Chen Y, Messerli SM, Mariggio MA, Rahner C, McNay E, Shore GC, Smith PJ, Hardwick JM, Jonas EA. Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase. Nature Cell Biology 2011, 13: 1224-1233. PMID: 21926988, PMCID: PMC3186867, DOI: 10.1038/ncb2330.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsbcl-2 Homologous Antagonist-Killer Proteinbcl-2-Associated X Proteinbcl-X ProteinBiphenyl CompoundsCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCells, CulturedEnergy MetabolismEnzyme InhibitorsHippocampusHydrolysisMembrane Potential, MitochondrialMitochondriaMitochondrial MembranesMitochondrial Proton-Translocating ATPasesNeuronsNitrophenolsOligomycinsOxygen ConsumptionPatch-Clamp TechniquesPiperazinesProton IonophoresRatsRecombinant Fusion ProteinsRNA InterferenceSulfonamidesSynapsesTime FactorsTransfectionConceptsBcl-xLSynthase complexATP synthaseMitochondrial F1Fo-ATP synthaseAnti-apoptotic BCL2 family proteinsF1Fo-ATP synthaseATP synthase complexF1FO-ATPase activityBcl-xL activityATPase activityBcl-xL proteinBCL2 family proteinsEndogenous Bcl-xLPresence of ATPFamily proteinsATPase complexNormal neuronal functionMembrane leak conductanceSubmitochondrial vesiclesΒ-subunitProtect cellsGenetic inhibitionMitochondrial efficiencyF1FoApoptotic molecules
2010
Synaptic Clustering of PSD-95 Is Regulated by c-Abl through Tyrosine Phosphorylation
de Arce K, Varela-Nallar L, Farias O, Cifuentes A, Bull P, Couch BA, Koleske AJ, Inestrosa NC, Alvarez AR. Synaptic Clustering of PSD-95 Is Regulated by c-Abl through Tyrosine Phosphorylation. Journal Of Neuroscience 2010, 30: 3728-3738. PMID: 20220006, PMCID: PMC2872795, DOI: 10.1523/jneurosci.2024-09.2010.Peer-Reviewed Original ResearchConceptsPSD-95Protein postsynaptic density protein 95Postsynaptic density protein 95PSD-95 clusteringHippocampal neuron culturesFirst postnatal weekC-AblC-Abl levelsPresynaptic markersTyrosine phosphorylationRat hippocampusPostnatal weekPostsynaptic sitesSynaptic clusteringNeuron culturesSynaptic functionC-Abl kinase activityReduced synapsesSynapse formationPostsynaptic compartmentsBrain synapsesGenetic inhibitionSynapsesTyrosine kinaseC-Abl tyrosine kinase
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