0000000000076616

AUTHOR

Zhenyue Hao

showing 2 related works from this author

In toxic demyelination oligodendroglial cell death occurs early and is FAS independent

2010

Oligodendroglial cell death is a frequent phenomenon of many neurological diseases, e.g. in demyelinating diseases such as multiple sclerosis (MS). The underlying mechanisms are largely unknown. Here, we demonstrate that in the toxic demyelination cuprizone model, oligodendroglial cell death and downregulation of myelin genes start days after initiation of the cuprizone diet and weeks before demyelination is obvious. In early – but not in later – stages, dying oligodendrocytes express activated caspase 3, suggesting a switch from classical apoptotic pathways to caspase 3-independent mechanisms during the course of the cuprizone diet. The expression level of FAS in the corpus callosum, a cel…

MaleProgrammed cell deathDown-RegulationMice TransgenicCaspase 3ApoptosisNerve Fibers MyelinatedArticleCorpus Callosumlcsh:RC321-571Mice03 medical and health sciencesMyelinCuprizone0302 clinical medicineDownregulation and upregulationmedicineAnimalsRNA Messengerfas Receptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCaspase030304 developmental biology0303 health sciencesCell DeathbiologyCaspase 3CytotoxinsMultiple sclerosisExperimental autoimmune encephalomyelitisFASmedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalOligodendrogliamedicine.anatomical_structureGene Expression RegulationNeurologyApoptosisMyelinImmunologybiology.proteinFemaleMyelin Proteins030217 neurology & neurosurgeryDemyelinating DiseasesSignal TransductionNeurobiology of Disease
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Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis.

2005

Abstract In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, immunization with myelin Ags leads to demyelination and paralysis. To investigate which molecules are crucial for the pathogenesis of EAE, we specifically assessed the roles of the death receptors Fas and TNF-R1. Mice lacking Fas expression in oligodendrocytes (ODCs) were generated and crossed to TNF-R1-deficient mice. To achieve specific deletion of a loxP-flanked fas allele in ODCs, we generated a new insertion transgene, expressing the Cre recombinase specifically in ODCs. Fas inactivation alone as well as the complete absence of TNF-R1 protected mice partially from EAE induced by the imm…

Encephalomyelitis Autoimmune ExperimentalEncephalomyelitisTransgeneT-LymphocytesImmunologyApoptosisMyelin oligodendrocyte glycoproteinMyelinInterferon-gammaMicemedicineImmunology and AllergyAnimalsfas ReceptorReceptorInflammationbiologyMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.diseaseMice Inbred C57BLMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologybiology.proteinInterleukin-2Myelin-Oligodendrocyte GlycoproteinMyelin ProteinsDemyelinating DiseasesJournal of immunology (Baltimore, Md. : 1950)
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