2025
Outer radial glia promotes white matter regeneration after neonatal brain injury
Jinnou H, Rosko L, Yamashita S, Henmi S, Prasad J, Lam V, Agaronyan A, Tu T, Imamura Y, Kuboyama K, Sawamoto K, Hashimoto-Torii K, Ishibashi N, Gallo V. Outer radial glia promotes white matter regeneration after neonatal brain injury. Cell Reports Medicine 2025, 6: 101986. PMID: 40023165, DOI: 10.1016/j.xcrm.2025.101986.Peer-Reviewed Original ResearchConceptsOuter radial gliaActivating transcription factor 5Oligodendrocyte precursor cellsTreating white matter injuryNeonatal brain injuryWhite matter injuryPeriventricular white matterWhite matter regenerationImprove functional recoveryPopulation of neural stem cellsNeural stem cellsBrain injuryOuter subventricular zoneSubventricular zoneProliferative capacityPostnatal developmentVentricular zoneFunctional recoveryPrecursor cellsStem cellsWhite matterRadial gliaTherapeutic targetNeonatal pigletsInjuryAn Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment
Gao D, Shipman W, Sun Y, Yang W, Mathew A, Beraki L, Glahn J, Kochen A, Kyriakides T, Horsley V, Hsia H. An Injectable Alginate Hydrogel Modified by Collagen and Fibronectin for Better Cellular Environment. ACS Applied Bio Materials 2025, 8: 1675-1683. PMID: 39886738, DOI: 10.1021/acsabm.4c01853.Peer-Reviewed Original ResearchMeSH KeywordsAlginatesAnimalsBiocompatible MaterialsCell ProliferationCollagenFibroblastsFibronectinsHumansHydrogelsMaterials TestingMiceParticle SizeConceptsEncapsulated fibroblastsAlginate hydrogelNeat alginate hydrogelsComposite hydrogelsModified hydrogelsInjectable hydrogelsStorage modulusMechanical propertiesCollagen hydrogelsMacroporous structureHydrogelsPore sizeAlginate functionalizationAlginate controlAlginate matrixAlginateFibroblast behaviorPro-angiogenic potentialFibroblast spreadingModulusPromote wound healingPoreFormation of fibrilsSLC25A38 is required for mitochondrial pyridoxal 5’-phosphate (PLP) accumulation
Pena I, Shi J, Chang S, Yang J, Block S, Adelmann C, Keys H, Ge P, Bathla S, Witham I, Sienski G, Nairn A, Sabatini D, Lewis C, Kory N, Vander Heiden M, Heiman M. SLC25A38 is required for mitochondrial pyridoxal 5’-phosphate (PLP) accumulation. Nature Communications 2025, 16: 978. PMID: 39856062, PMCID: PMC11760969, DOI: 10.1038/s41467-025-56130-3.Peer-Reviewed Original ResearchConceptsPyridoxal 5'-phosphateGenome-wide CRISPR interference screenPyridoxal 5'-phosphate-dependent enzymeCRISPR interference screenSerine hydroxymethyltransferase-2Active form of vitamin B6One-carbon unitsImpaired cellular proliferationAmino acid metabolismOne-carbon metabolismInterference screenEssential proteinsMolecular machineryNucleotide synthesisCongenital sideroblastic anemiaProliferation defectSLC25A38Acid metabolismErythroleukemia cellsOrnithine aminotransferaseActive formK562 cellsEnzymatic reactionsCellular proliferationPolyamine synthesisSignificance of birth in the maintenance of quiescent neural stem cells
Kawase K, Nakamura Y, Wolbeck L, Takemura S, Zaitsu K, Ando T, Jinnou H, Sawada M, Nakajima C, Rydbirk R, Gokenya S, Ito A, Fujiyama H, Saito A, Iguchi A, Kratimenos P, Ishibashi N, Gallo V, Iwata O, Saitoh S, Khodosevich K, Sawamoto K. Significance of birth in the maintenance of quiescent neural stem cells. Science Advances 2025, 11: eadn6377. PMID: 39841848, PMCID: PMC11753423, DOI: 10.1126/sciadv.adn6377.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBrainCell ProliferationEpendymoglial CellsFemaleGlutamineMiceNeural Stem CellsNeurogenesisParturitionConceptsNeural stem cellsQuiescent neural stem cellsStem cellsRadial gliaNeural stem cell poolAcquisition of quiescenceEmbryonic neural stem cellsPreterm birthPostnatal neural stem cellsCellular processesPostnatal neurogenesisGlutamine metabolismPostnatal brainLong-term maintenanceDevelopmental processesBirthNeurogenesisPretermCells
2024
Development of a small molecule-based two-photon photosensitizer for targeting cancer cells
Lee D, Cao Y, Juvekar V, Sauraj, Noh C, Shin S, Liu Z, Kim H. Development of a small molecule-based two-photon photosensitizer for targeting cancer cells. Journal Of Materials Chemistry B 2024, 12: 12232-12238. PMID: 39469993, DOI: 10.1039/d4tb01706d.Peer-Reviewed Original ResearchConceptsTarget cancer cellsReactive oxygen speciesPhotodynamic therapyCancer cellsDiverse cell linesInduced ROS productionColon cancer tissuesTwo-photon (TPCell deathLow dark toxicityCancer modelsTwo-photon photosensitizerROS productionCancer selectivityInduce cell damageThree-dimensional spheroidsCell linesTP excitationImaging-guided photodynamic therapyCancer tissuesOxygen speciesTP-PDTEzrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktA proteogenomic analysis of cervical cancer reveals therapeutic and biological insights
Yu J, Gui X, Zou Y, Liu Q, Yang Z, An J, Guo X, Wang K, Guo J, Huang M, Zhou S, Zuo J, Chen Y, Deng L, Yuan G, Li N, Song Y, Jia J, Zeng J, Zhao Y, Liu X, Du X, Liu Y, Wang P, Zhang B, Ding L, Robles A, Rodriguez H, Zhou H, Shao Z, Wu L, Gao D. A proteogenomic analysis of cervical cancer reveals therapeutic and biological insights. Nature Communications 2024, 15: 10114. PMID: 39578447, PMCID: PMC11584810, DOI: 10.1038/s41467-024-53830-0.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAdultBiomarkers, TumorCell Line, TumorCell ProliferationE1A-Associated p300 ProteinFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedPapillomaviridaePapillomavirus InfectionsPrognosisProtein Kinase C betaProtein Processing, Post-TranslationalProteogenomicsProto-Oncogene Proteins c-fosUterine Cervical NeoplasmsConceptsCervical cancerIncidence of cervical cancerIntegrative proteogenomic analysisMulti-omic changesHuman papillomavirusImmune infiltrationSignificant public health issueProteogenomic analysisGenetic alterationsCC patientsPatient subgroupsMalignant proliferationAnalysis of cervical cancerCC tumorsChinese womenPost-translational modifications regulationPublic health issuePotential treatmentScreening strategiesClinical practiceProliferation of CC cellsPatientsWomen's healthCancerLow-income countriesG9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1
Exposito F, Redrado M, Serrano D, Calabuig-Fariñas S, Bao-Caamano A, Gallach S, Jantus-Lewintre E, Diaz-Lagares A, Rodriguez-Casanova A, Sandoval J, San Jose-Eneriz E, Garcia J, Redin E, Senent Y, Leon S, Pio R, Lopez R, Oyarzabal J, Pineda-Lucena A, Agirre X, Montuenga L, Prosper F, Calvo A. G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1. Cell Death & Disease 2024, 15: 787. PMID: 39488528, PMCID: PMC11531574, DOI: 10.1038/s41419-024-07156-w.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerNon-small cell lung cancer patientsCM-272Treatment of non-small cell lung cancerReprogram tumor cellsAssociated with poor prognosisResponse to chemotherapyCell lung cancerCancer drugsMonitor tumor progressionOverexpression of G9aNSCLC cell linesLung cancer growthCancer drug sensitivityNon-small cell lung cancer growthNon-invasive biomarkersTumor volumeAntitumor efficacyTargeted therapyPoor prognosisCancer modelsTumor cellsInduce cell deathTumor progressionLung cancerMitochondrial reprogramming by activating OXPHOS via glutamine metabolism in African American patients with bladder cancer
Reddy K, Piyarathna D, Park J, Putluri V, Amara C, Kamal A, Xu J, Kraushaar D, Huang S, Jung S, Eberlin L, Johnson J, Kittles R, Ballester L, Parsawar K, Siddiqui M, Gao J, Gramer A, Bollag R, Terris M, Lotan Y, Creighton C, Lerner S, Sreekumar A, Kaipparettu B, Putluri N. Mitochondrial reprogramming by activating OXPHOS via glutamine metabolism in African American patients with bladder cancer. JCI Insight 2024, 9: e172336. PMID: 39253977, PMCID: PMC11385078, DOI: 10.1172/jci.insight.172336.Peer-Reviewed Original ResearchConceptsBladder cancerOxidative phosphorylationComponents of complex IComplex IElevated mitochondrial oxidative phosphorylationComprehensive RNA-seqReduced basal respirationActive oxidative phosphorylationMitochondrial oxidative phosphorylationDecreased tumor growthTumor growth potentialIncreased disease progressionMitochondrial respiration rateAfrican American patientsRNA-seqRace-specific differencesMitochondrial reprogrammingEuropean AmericansMetabolic rewiringOXPHOS activityBasal respirationGlutamine metabolismGLS1 expressionPreclinical studiesATP productionPreclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer
Hartwich T, Mansolf M, Demirkiran C, Greenman M, Bellone S, McNamara B, Nandi S, Alexandrov L, Yang‐Hartwich Y, Coma S, Pachter J, Santin A. Preclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer. Cancer Medicine 2024, 13: e70210. PMID: 39240189, PMCID: PMC11378359, DOI: 10.1002/cam4.70210.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCarcinoma, EndometrioidCell Line, TumorCell ProliferationEndometrial NeoplasmsExome SequencingFemaleFocal Adhesion Kinase 1HumansImidazolesMiceNeoplasm GradingOxazepinesProtein Kinase InhibitorsPyrazinesSulfonamidesXenograft Model Antitumor AssaysConceptsFocal adhesion kinaseWhole-exome sequencingEndometrial cancer cell linesVS-4718Cell linesRas/MAPK pathwayPhosphorylated focal adhesion kinaseWestern blot assayWhole-exome sequencing resultsRAF/MEK inhibitionEAC cell linesBlot assayP-FAKGenetic landscapeCell cycleEndometrial cancerGenetic derangementsDefactinibP-MEKGrowth inhibitionRAF/MEKRas/MAPKCell viabilityP-ERKHigh-grade endometrial cancerStatins Inhibit Cutaneous Squamous Cell Carcinoma Cells
HACKETT A, COHEN A, RUTENBERG T, HODAK E, MOYAL L, ATZMONY L. Statins Inhibit Cutaneous Squamous Cell Carcinoma Cells. Acta Dermato Venereologica 2024, 104: 25097. PMID: 39185545, PMCID: PMC11367778, DOI: 10.2340/actadv.v104.25097.Peer-Reviewed Original ResearchCRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma
Cui M, Liu Z, Wang S, Bae S, Guo H, Zhou J, Liu R, Wang L. CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma. Oncogene 2024, 43: 2708-2721. PMID: 39112518, PMCID: PMC11364504, DOI: 10.1038/s41388-024-03115-z.Peer-Reviewed Original ResearchConceptsMiR-23aMiR-27aCRISPR interferenceCRISPR activationHigh-throughput RNA-seqCell migrationCDK1/cyclin B activityReduced cell growth in vitroMiRNA target predictionCell cycle arrestMiRNA clusterHepatocellular carcinoma cellsCell growth in vitroRNA-seqGene networksTarget predictionCRISPR knockoutOncogenic roleGrowth in vitroCycle arrestMature miRNAsMiRNAsG2/M phaseSignaling pathwayOncogenic functionAcyl-CoA Synthetase Medium-Chain Family Member 5–Mediated Fatty Acid Metabolism Dysregulation Promotes the Progression of Hepatocellular Carcinoma
Yang L, Pham K, Xi Y, Jiang S, Robertson K, Liu C. Acyl-CoA Synthetase Medium-Chain Family Member 5–Mediated Fatty Acid Metabolism Dysregulation Promotes the Progression of Hepatocellular Carcinoma. American Journal Of Pathology 2024, 194: 1951-1966. PMID: 39069168, PMCID: PMC11423759, DOI: 10.1016/j.ajpath.2024.07.002.Peer-Reviewed Original ResearchConceptsDNA methyltransferase 1Fatty acid metabolismAcyl-CoADown-regulationAcid metabolismDecreased STAT3 phosphorylationCell linesPromoter region methylationHepatocellular carcinoma cell lineHepatocellular carcinoma patient samplesDNA methylationFatty acid accumulationDysregulated fatty acid metabolismSTAT3 phosphorylationDecreased cell proliferationHepatocellular carcinomaHepatocellular carcinoma tumor tissuesMethyltransferase 1Region methylationRegulatory mechanismsACSM5Molecular mechanismsMetabolic dysregulationProgression of hepatocellular carcinomaAcid accumulationA metabolic dependency of EBV can be targeted to hinder B cell transformation
Müller-Durovic B, Jäger J, Engelmann C, Schuhmachers P, Altermatt S, Schlup Y, Duthaler U, Makowiec C, Unterstab G, Roffeis S, Xhafa E, Assmann N, Trulsson F, Steiner R, Edwards-Hicks J, West J, Turner L, Develioglu L, Ivanek R, Azzi T, Dehio P, Berger C, Kuzmin D, Saboz S, Mautner J, Löliger J, Geigges M, Palianina D, Khanna N, Dirnhofer S, Münz C, Bantug G, Hess C, Berger C, Hess C, Koller M, Rossi S, Stampf S, Müller N. A metabolic dependency of EBV can be targeted to hinder B cell transformation. Science 2024, 385: eadk4898. PMID: 38781354, DOI: 10.1126/science.adk4898.Peer-Reviewed Original ResearchConceptsEpstein-Barr virusIndoleamine 2,3-dioxygenase 1B-cell transformationB cellsEBV-driven B-cell transformationIndoleamine 2,3-dioxygenase 1 expressionIndoleamine 2,3-dioxygenase 1 inhibitionInfection of B cellsEBV-infected B cellsEnzyme indoleamine 2,3-dioxygenase 1Epstein-Barr virus protein EBNA2Increased IDO1 activityNicotinamide adenine dinucleotideDevelopment of lymphomaEBV-related diseasesInfected B cellsHumanized miceTransplant patientsImmune dysregulationAdenosine triphosphateMitochondrial complex I activityComplex I activityMetabolic vulnerabilitiesIDO1 activitySerum signatureGrowth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex
Aladelokun O, Lu L, Zheng J, Yan H, Jain A, Gibson J, Khan S, Johnson C. Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex. Human Genomics 2024, 18: 67. PMID: 38886847, PMCID: PMC11184737, DOI: 10.1186/s40246-024-00635-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAspartate-Ammonia LigaseCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHeterograftsHumansMaleMiceReceptors, EstrogenReceptors, G-Protein-CoupledSex FactorsXenograft Model Antitumor AssaysConceptsFemale tumor-bearing miceFemale CRC patientsTumor-bearing miceCRC patientsTumor growthInferior survivalAssociated with inferior survivalMetabolic reprogrammingG protein-coupled estrogen receptorTriggering metabolic reprogrammingSustained tumor growthSuppressed tumor growthExpression of asparagine synthetaseCancer cell linesBackgroundSex-related differencesSurvival improvementImpact of sexFemale miceEstrogen receptorCancer growthTranslational relevanceRewiring of metabolic pathwaysCancer burdenMetabolic pathwaysAsparagine synthetaseNotch signaling regulates UNC5B to suppress endothelial proliferation, migration, junction activity, and retinal plexus branching
Raza Q, Nadeem T, Youn S, Swaminathan B, Gupta A, Sargis T, Du J, Cuervo H, Eichmann A, Ackerman S, Naiche L, Kitajewski J. Notch signaling regulates UNC5B to suppress endothelial proliferation, migration, junction activity, and retinal plexus branching. Scientific Reports 2024, 14: 13603. PMID: 38866944, PMCID: PMC11169293, DOI: 10.1038/s41598-024-64375-z.Peer-Reviewed Original ResearchConceptsNotch signalingEndothelial cell behaviorEndothelial junctionsCell behaviorMultiple endothelial cell typesStabilization of endothelial junctionsNotch activationEndothelial Notch signalingTarget of Notch signalingTranscriptional activation complexEndothelial cell typesPlexus branchesVascular densityEndothelial proliferationBrain endotheliumMouse retinaIn vivo targetingEffector proteinsVascular outgrowthJunction activityNotch proteinsEndothelial cellsExcessive vascularizationDownstream effectorsEndothelial gene expressionTert-expressing cells contribute to salivary gland homeostasis and tissue regeneration after radiation therapy
Guan L, Viswanathan V, Jiang Y, Vijayakumar S, Cao H, Zhao J, Colburg D, Neuhöfer P, Zhang Y, Wang J, Xu Y, Laseinde E, Hildebrand R, Rahman M, Frock R, Kong C, Beachy P, Artandi S, Le Q. Tert-expressing cells contribute to salivary gland homeostasis and tissue regeneration after radiation therapy. Genes & Development 2024, 38: 569-582. PMID: 38997156, PMCID: PMC11293384, DOI: 10.1101/gad.351577.124.Peer-Reviewed Original ResearchConceptsSubmandibular glandSalivary gland homeostasisProgenitor cellsGland homeostasisResponse to radiotherapyAdult submandibular glandCell survivalSalivary gland regenerationSelf-renewal capacityEnhanced proliferative activityRadiation therapyDuctal regionsRadiotherapyModulate cell survivalTelomerase-expressingGland regenerationProliferative activityMouse strainsTERT expressionCreERT2 recombinaseSalivary gland biologyRadiation exposureTERT locusIn vitro cultureCell populationsIn silico model development and optimization of in vitro lung cell population growth
Mostofinejad A, Romero D, Brinson D, Marin-Araujo A, Bazylak A, Waddell T, Haykal S, Karoubi G, Amon C. In silico model development and optimization of in vitro lung cell population growth. PLOS ONE 2024, 19: e0300902. PMID: 38748626, PMCID: PMC11095723, DOI: 10.1371/journal.pone.0300902.Peer-Reviewed Original ResearchMeSH KeywordsCell LineCell ProliferationComputer SimulationEpithelial CellsGlucoseHumansLungModels, BiologicalOxygenTissue EngineeringBone marrow mesenchymal stem cell-derived exosomes shuttle microRNAs to endometrial stromal fibroblasts that promote tissue proliferation /regeneration/ and inhibit differentiation
Bonavina G, Mamillapalli R, Krikun G, Zhou Y, Gawde N, Taylor H. Bone marrow mesenchymal stem cell-derived exosomes shuttle microRNAs to endometrial stromal fibroblasts that promote tissue proliferation /regeneration/ and inhibit differentiation. Stem Cell Research & Therapy 2024, 15: 129. PMID: 38693588, PMCID: PMC11064399, DOI: 10.1186/s13287-024-03716-1.Peer-Reviewed Original ResearchMeSH KeywordsBone Marrow CellsCell DifferentiationCell ProliferationEndometriumExosomesFemaleFibroblastsHumansMesenchymal Stem CellsMicroRNAsRegenerationConceptsMiR-100-5pMiR-100MiR-21Transmission electron microscopyMiR-143MiR-143-3pMiR-21-5pEndometrial stromal fibroblastsStromal fibroblastsMicroRNAsExtracellular vesiclesElectron microscopyCell-free regenerative therapyNanoparticle tracking analysisMiRNAsBone marrow mesenchymal stem cell-derived exosomesBone marrow-derived stem cellsMesenchymal stem cell-derived exosomesStem cell-derived exosomesDelivery of microRNAsMarrow-derived stem cellsAssociated with several signaling pathwaysMediators of tissue repairMethodsExtracellular vesiclesUnpaired t-testTRPM7 facilitates fibroblast-like synoviocyte proliferation, metastasis and inflammation through increasing IL-6 stability via the PKCα-HuR axis in rheumatoid arthritis
Lin Y, Chen Y, Hu W, Liu X, Hao W, Xing J, Ding J, Xu Y, Yao F, Zhao Y, Wang K, Li S, Yu Q, Hu W, Zhou R. TRPM7 facilitates fibroblast-like synoviocyte proliferation, metastasis and inflammation through increasing IL-6 stability via the PKCα-HuR axis in rheumatoid arthritis. International Immunopharmacology 2024, 132: 111933. PMID: 38581988, DOI: 10.1016/j.intimp.2024.111933.Peer-Reviewed Original ResearchConceptsTransient receptor potential melastatin 7Rheumatoid arthritisInhibition of transient receptor potential melastatin 7Human RA patientsSynovial hyperplasiaAdjuvant-induced arthritis ratsIncreased TRPM7 expressionIL-6 mRNATreatment of RAPathogenesis of RAFibroblast-like synoviocytesTRPM7 silencingProgression of rheumatoid arthritisTRPM7 expressionChannel inhibitionCation channelsRA patientsMetastasisPharmacological inhibitionArthritis ratsInflammationNuclear translocationSynoviocyte proliferationHyperplasiaProliferation
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