2024
Meningeal lymphatic vessel dysfunction driven by CGRP signaling causes migraine-like pain in mice
Thomas J, Schindler E, Gottschalk C. Meningeal lymphatic vessel dysfunction driven by CGRP signaling causes migraine-like pain in mice. Journal Of Clinical Investigation 2024, 134: e182556. PMID: 39087472, PMCID: PMC11290958, DOI: 10.1172/jci182556.Peer-Reviewed Original ResearchConceptsBlocking CGRP signalingCGRP receptor componentsMigraine-like painCervical lymph nodesGap junction proteinPrimary headache disordersLymphatic vessel dysfunctionAcute migrainePharmacological blockadeLymph nodesHeadache disordersNeurological symptomsJunction proteinsCGRPLymphatic vesselsMeningeal lymphatic vesselsInducible knockoutVessel dysfunctionMigraineReceptor componentsHeadachePainPathophysiologyDysfunctionMice
2019
Endophilin-A2 dependent VEGFR2 endocytosis promotes sprouting angiogenesis
Genet G, Boyé K, Mathivet T, Ola R, Zhang F, Dubrac A, Li J, Genet N, Henrique Geraldo L, Benedetti L, Künzel S, Pibouin-Fragner L, Thomas JL, Eichmann A. Endophilin-A2 dependent VEGFR2 endocytosis promotes sprouting angiogenesis. Nature Communications 2019, 10: 2350. PMID: 31138815, PMCID: PMC6538628, DOI: 10.1038/s41467-019-10359-x.Peer-Reviewed Original ResearchMeSH KeywordsAcyltransferasesAnimalsCell MovementCell PolarityCell ProliferationCell SurvivalEndocytosisEndothelial CellsIntercellular Signaling Peptides and ProteinsMAP Kinase Signaling SystemMiceMice, KnockoutNeovascularization, PhysiologicNerve Tissue ProteinsP21-Activated KinasesReceptors, ImmunologicRetinal VesselsVascular Endothelial Growth Factor Receptor-2ConceptsEndophilin A2Endothelial cell migrationSprouting angiogenesisCell migrationFront-rear polarityBAR domain proteinsFront-rear polarizationClathrin-independent internalizationSpecific endocytic pathwaysVEGFR2 endocytosisEndocytic pathwayAngiogenesis defectsEffector PAKTip cellsSlit-RoboActivation of VEGFR2Downstream activationVEGFR2 internalizationCell behaviorPathological angiogenesisCritical mediatorEndocytosisPathological conditions
2018
Oligodendrocyte precursor survival and differentiation requires chromatin remodeling by Chd7 and Chd8
Marie C, Clavairoly A, Frah M, Hmidan H, Yan J, Zhao C, Van Steenwinckel J, Daveau R, Zalc B, Hassan B, Thomas JL, Gressens P, Ravassard P, Moszer I, Martin DM, Lu QR, Parras C. Oligodendrocyte precursor survival and differentiation requires chromatin remodeling by Chd7 and Chd8. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 115: e8246-e8255. PMID: 30108144, PMCID: PMC6126750, DOI: 10.1073/pnas.1802620115.Peer-Reviewed Original ResearchConceptsChromatin remodelersProliferation-differentiation balanceNormal developmentChromatin accessibility analysisOligodendrocyte precursor cellsChromatin closingChromatin remodelingChromatin openingTranscriptional repressionGenetic interactionsUncharacterized functionGenetic reprogrammingRisk-associated genesTranscriptional activationKey regulatorNeurodevelopmental defectsPrecursor survivalLineage cellsCHD7RemodelersOligodendrocyte lineage cellsPrecursor cellsGlioma formationBinding profileCHD8
2015
Targeting NCK-Mediated Endothelial Cell Front-Rear Polarity Inhibits Neovascularization
Dubrac A, Genet G, Ola R, Zhang F, Pibouin-Fragner L, Han J, Zhang J, Thomas JL, Chedotal A, Schwartz MA, Eichmann A. Targeting NCK-Mediated Endothelial Cell Front-Rear Polarity Inhibits Neovascularization. Circulation 2015, 133: 409-421. PMID: 26659946, PMCID: PMC4729599, DOI: 10.1161/circulationaha.115.017537.Peer-Reviewed Original ResearchConceptsFront-rear polaritySprouting angiogenesisSignal integration mechanismImportant drug targetsNck adaptorsCytoskeletal dynamicsEndothelial cell migrationEmbryonic developmentAngiogenesis defectsPAK2 activationVessel sproutsNumber of diseasesBlood vessel growthDrug targetsCell migrationPostnatal retinaAngiogenic growthNckNck1AdaptorVessel growthKey processesEndothelial cellsPathological ocular neovascularizationInhibits neovascularization
2014
Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1
Patterson VL, Zullo AJ, Koenig C, Stoessel S, Jo H, Liu X, Han J, Choi M, DeWan AT, Thomas JL, Kuan CY, Hoh J. Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1. PLOS ONE 2014, 9: e115789. PMID: 25531304, PMCID: PMC4274161, DOI: 10.1371/journal.pone.0115789.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBehavior, AnimalBlotting, WesternCell ProliferationCerebellumFemaleGTP PhosphohydrolasesHigh-Temperature Requirement A Serine Peptidase 2MaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial ProteinsNerve DegenerationNeuronsParkinson DiseaseReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence DeletionSerine EndopeptidasesSignal TransductionConceptsNeural-specific deletionStriatal neuronal lossPostnatal day 18Days of ageNeuronal lossNeurological symptomsParkinson's diseaseMouse modelParkinsonian phenotypeSystemic effectsMitochondrial Opa1Day 18Premature deathMutant miceNeural contributionsMiceCerebellar neurodegenerationKey moleculesStructural anomaliesAbnormal activityAbnormal morphologyCerebellumDiseaseComplete penetranceDeath
2013
Ascl1/Mash1 Promotes Brain Oligodendrogenesis during Myelination and Remyelination
Nakatani H, Martin E, Hassani H, Clavairoly A, Maire CL, Viadieu A, Kerninon C, Delmasure A, Frah M, Weber M, Nakafuku M, Zalc B, Thomas JL, Guillemot F, Nait-Oumesmar B, Parras C. Ascl1/Mash1 Promotes Brain Oligodendrogenesis during Myelination and Remyelination. Journal Of Neuroscience 2013, 33: 9752-9768. PMID: 23739972, PMCID: PMC3892435, DOI: 10.1523/jneurosci.0805-13.2013.Peer-Reviewed Original ResearchConceptsOligodendrocyte precursor cellsNeonatal periodCortical oligodendrocyte precursor cellsOligodendrocyte developmentCortical subventricular zoneSubventricular zone progenitorsMultiple sclerosis lesionsMyelin-forming cellsPostnatal cortexRemyelination processFocal demyelinationCorpus callosumSubventricular zoneOPC differentiationPostnatal brainMouse modelAscl1 functionOligodendrogenesisOPC developmentSclerosis lesionsASCL1 expressionCortical progenitorsRemyelinationProneural transcription factorsOligodendrocytes
2012
Opposing Roles for Hoxa2 and Hoxb2 in Hindbrain Oligodendrocyte Patterning
Miguez A, Ducret S, Di Meglio T, Parras C, Hmidan H, Haton C, Sekizar S, Mannioui A, Vidal M, Kerever A, Nyabi O, Haigh J, Zalc B, Rijli FM, Thomas JL. Opposing Roles for Hoxa2 and Hoxb2 in Hindbrain Oligodendrocyte Patterning. Journal Of Neuroscience 2012, 32: 17172-17185. PMID: 23197710, PMCID: PMC6621859, DOI: 10.1523/jneurosci.0885-12.2012.Peer-Reviewed Original ResearchSemaphorin3A, Neuropilin-1, and PlexinA1 Are Required for Lymphatic Valve Formation
Bouvrée K, Brunet I, del Toro R, Gordon E, Prahst C, Cristofaro B, Mathivet T, Xu Y, Soueid J, Fortuna V, Miura N, Aigrot MS, Maden CH, Ruhrberg C, Thomas JL, Eichmann A. Semaphorin3A, Neuropilin-1, and PlexinA1 Are Required for Lymphatic Valve Formation. Circulation Research 2012, 111: 437-445. PMID: 22723296, PMCID: PMC3861899, DOI: 10.1161/circresaha.112.269316.Peer-Reviewed Original ResearchAnimalsAnimals, NewbornAntibodies, NeutralizingBacterial ProteinsCells, CulturedEndothelial CellsGene Expression Regulation, DevelopmentalGenotypeGestational AgeHumansLuminescent ProteinsLymphatic VesselsMiceMice, KnockoutMice, TransgenicMorphogenesisNerve Tissue ProteinsNeuropilin-1PhenotypeReceptors, Cell SurfaceRNA, MessengerSemaphorin-3AVascular Endothelial Growth Factor Receptor-3
2011
A complex between contactin-1 and the protein tyrosine phosphatase PTPRZ controls the development of oligodendrocyte precursor cells
Lamprianou S, Chatzopoulou E, Thomas J, Bouyain S, Harroch S. A complex between contactin-1 and the protein tyrosine phosphatase PTPRZ controls the development of oligodendrocyte precursor cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 17498-17503. PMID: 21969550, PMCID: PMC3198311, DOI: 10.1073/pnas.1108774108.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCell DifferentiationCell ProliferationContactin 1Crystallography, X-RayHumansMiceMice, KnockoutModels, MolecularModels, NeurologicalMultiprotein ComplexesNeural Stem CellsNeurogenesisOligodendrogliaProtein Structure, TertiaryReceptor-Like Protein Tyrosine Phosphatases, Class 5Recombinant ProteinsSolubilityConceptsCarbonic anhydrase-like domainPrecursor cellsReceptor protein tyrosineOligodendrocyte precursor cellsPtprz-deficient miceProtein tyrosineCell adhesion moleculeNeural cell adhesion moleculeBiological roleContactin familyCocrystal structureGlial cell populationsUnknown modulatorsPtprzCentral nervous systemCell populationsCNTN1Structural dataAdhesion moleculesBindsContactin-1CellsMature oligodendrocytesComplexesNervous system
2008
Structural Requirement of TAG-1 for Retinal Ganglion Cell Axons and Myelin in the Mouse Optic Nerve
Chatzopoulou E, Miguez A, Savvaki M, Levasseur G, Muzerelle A, Muriel M, Goureau O, Watanabe K, Goutebroze L, Gaspar P, Zalc B, Karagogeos D, Thomas J. Structural Requirement of TAG-1 for Retinal Ganglion Cell Axons and Myelin in the Mouse Optic Nerve. Journal Of Neuroscience 2008, 28: 7624-7636. PMID: 18650339, PMCID: PMC6670848, DOI: 10.1523/jneurosci.1103-08.2008.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAxonsCell Adhesion Molecules, NeuronalCells, CulturedContactin 2Embryo, MammalianGene Expression Regulation, DevelopmentalLeukocyte L1 Antigen ComplexMiceMice, KnockoutMyelin SheathNerve Tissue ProteinsNeurogliaOptic NerveRetinaRetinal Ganglion CellsTranscription Factor Brn-3AConceptsOptic nerveRetinal ganglion cellsRGC axonsTAG-1Retinal ganglion cell axonsEmbryonic retinal ganglion cellsGanglion cell axonsMouse optic nerveLateral geniculate nucleusWhite matter axonsMyelin-forming cellsPersistent abnormalitiesGanglion cellsGlial cellsCell adhesion moleculeContralateral projectionsGeniculate nucleusCell axonsAstroglial networksRetinal axonsNerveAxonal tractsAxonal caliberMyelination defectsAxons
2006
VEGF-C is a trophic factor for neural progenitors in the vertebrate embryonic brain
Le Bras B, Barallobre MJ, Homman-Ludiye J, Ny A, Wyns S, Tammela T, Haiko P, Karkkainen MJ, Yuan L, Muriel MP, Chatzopoulou E, Bréant C, Zalc B, Carmeliet P, Alitalo K, Eichmann A, Thomas JL. VEGF-C is a trophic factor for neural progenitors in the vertebrate embryonic brain. Nature Neuroscience 2006, 9: 340-348. PMID: 16462734, DOI: 10.1038/nn1646.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCell DifferentiationCells, CulturedEvolution, MolecularIntermediate Filament ProteinsLarvaLateral VentriclesMiceMice, KnockoutMice, TransgenicNerve Growth FactorsNerve Tissue ProteinsNestinNeuronsOligodendrogliaOptic NerveRatsRats, WistarStem CellsVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-3Xenopus laevisConceptsNeural progenitor cellsReceptor VEGFR-3Mouse embryosNeural progenitorsVEGFR-3Progenitor cellsVertebrate embryonic brainBlood vessel defectsOligodendrocyte precursor cellsXenopus laevisAction of VEGFEmbryonic brainVascular endothelial growth factor CVEGF-C knockdownNeural cellsPrecursor cellsVessel defectsFactor CEmbryosGrowth factorProgenitorsCellsProliferation of OPCsVascular systemLymphatic vessels