Search results for "Neuroepithelial Cells"

showing 4 items of 4 documents

Different immunohistochemical levels of Hsp60 and Hsp70 in a subset of brain tumors and putative role of Hsp60 in neuroepithelial tumorigenesis

2013

In this work we analysed, by immunohistochemistry, a series of brain tumors to detect the levels and cellular distribution of Hsp60 and Hsp70. We found that Hsp60 levels were significantly higher than those of Hsp70 in neuroepithelial tumors, while levels of both molecules were not significantly different from each other in meningeal neoplasms. In particular, Hsp60 immunopositivity was present mainly at the cytoplasmic level, while Hsp70 immunopositivity was found both in the cytoplasm and in the nucleus of tumor cells. The levels of these molecules in healthy control cells were always very low. Finally, Hsp60 and Hsp70 levels did not correlate with the different types (WHO grade) of neopla…

AdultMalePathologymedicine.medical_specialtyanimal structuresHistologyAdolescentNeuroepithelial CellsBiophysicschemical and pharmacologic phenomenaBiologymedulloblastomamedicine.disease_causemeningiomacomplex mixturesHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningiomaHsp70Meningeal NeoplasmsmedicineHumansHSP70 Heat-Shock ProteinsMeningeal NeoplasmChildastrocytomalcsh:QH301-705.5AgedAged 80 and overMedulloblastomaHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningioma.Brain NeoplasmsBrief ReportfungiAstrocytomaChaperonin 60Cell BiologyMiddle AgedHsp60medicine.diseaseImmunohistochemistryNeoplasms NeuroepithelialNeuroepithelial cellglioblastoma multiformaelcsh:Biology (General)Tumor progressionChild PreschoolCancer cellImmunohistochemistryFemaleCarcinogenesisEuropean Journal of Histochemistry
researchProduct

Dystroglycan regulates structure, proliferation and differentiation of neuroepithelial cells in the developing vertebrate CNS.

2007

AbstractIn the developing CNS α- and β-dystroglycan are highly concentrated in the endfeet of radial neuroepithelial cells at the contact site to the basal lamina. We show that injection of anti-dystroglycan Fab fragments, knockdown of dystroglycan using RNAi, and overexpression of a dominant-negative dystroglycan protein by microelectroporation in neuroepithelial cells of the chick retina and optic tectum in vivo leads to the loss of their radial morphology, to hyperproliferation, to an increased number of postmitotic neurons, and to an altered distribution of several basally concentrated proteins. Moreover, these treatments also altered the oriented growth of axons from retinal ganglion c…

musculoskeletal diseasesCentral Nervous Systemcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtySuperior Colliculianimal structuresCellular differentiationNeuroepithelial CellsStem cellsDevelopmentDystrophin-associated protein complexRetinal ganglionAxonal growthMuscular DystrophiesRetina03 medical and health sciences0302 clinical medicineInternal medicineDystroglycanmedicineAnimalsDystroglycansMolecular BiologyCell Shape030304 developmental biologyCell Proliferation0303 health sciencesRetinabiologyfungiCell DifferentiationCell BiologyMuscular dystrophymusculoskeletal systemCell biologyNeuroepithelial cellmedicine.anatomical_structureEndocrinologyRNAiVertebratesbiology.proteinBasal laminaPikachurinStem cellChickens030217 neurology & neurosurgeryDevelopmental BiologyDevelopmental biology
researchProduct

An essential switch in subunit composition of a chromatin remodeling complex during neural development.

2007

Summary Mammalian neural stem cells (NSCs) have the capacity to both self-renew and to generate all the neuronal and glial cell-types of the adult nervous system. Global chromatin changes accompany the transition from proliferating NSCs to committed neuronal lineages, but the mechanisms involved have been unclear. Using a proteomics approach, we show that a switch in subunit composition of neural, ATP-dependent SWI/SNF-like chromatin remodeling complexes accompanies this developmental transition. Proliferating neural stem and progenitor cells express complexes in which BAF45a, a Kruppel/PHD domain protein and the actin-related protein BAF53a are quantitatively associated with the SWI2/SNF2-…

Cellular differentiationProtein subunitNeuroscience(all)Molecular Sequence DataNeuroepithelial CellsDEVBIONerve Tissue ProteinsBiologyChromatin remodelingMOLNEUROEpigenesis Genetic03 medical and health sciencesMice0302 clinical medicineMultienzyme ComplexesAnimalsAmino Acid SequenceProgenitor cell030304 developmental biologyNeurons0303 health sciencesGeneral NeuroscienceMultipotent Stem CellsGene Expression Regulation DevelopmentalCell DifferentiationChromatin Assembly and DisassemblySTEMCELLNeural stem cellChromatinCell biologyNeuroepithelial cellProtein SubunitsNeural developmentNeuroglia030217 neurology & neurosurgeryTranscription FactorsNeuron
researchProduct

Sustained activation of mTOR pathway in embryonic neural stem cells leads to development of tuberous sclerosis complex-associated lesions

2011

SummaryTuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by hamartomatous neurological lesions that exhibit abnormal cell proliferation and differentiation. Hyperactivation of mTOR pathway by mutations in either the Tsc1 or Tsc2 gene underlies TSC pathogenesis, but involvement of specific neural cell populations in the formation of TSC-associated neurological lesions remains unclear. We deleted Tsc1 in Emx1-expressing embryonic telencephalic neural stem cells (NSCs) and found that mutant mice faithfully recapitulated TSC neuropathological lesions, such as cortical lamination defects and subependymal nodules (SENs). These alterations were caused by enhanced gen…

Telencephaloncongenital hereditary and neonatal diseases and abnormalitiesCellular differentiationNeuroepithelial CellsEmbryonic DevelopmentBiologyTuberous Sclerosis Complex 1 Proteinmurine modelCerebral VentriclesMiceNeural Stem CellsCell MovementTuberous SclerosismedicineGeneticsAnimalsAnimals; Animals Newborn; Cell Differentiation; Cell Movement; Cell Proliferation; Cerebral Ventricles; Embryonic Development; Embryonic Stem Cells; Epilepsy; Gene Silencing; Gene Targeting; Megalencephaly; Mice; Mutation; Neural Stem Cells; Neuroepithelial Cells; Neurons; TOR Serine-Threonine Kinases; Telencephalon; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins; Signal TransductionGene SilencingNeural cellPI3K/AKT/mTOR pathwayEmbryonic Stem CellsCell ProliferationNeuronsEpilepsymTOR; Neural Stem Cells; Tuberous Sclerosis; murine modelTOR Serine-Threonine KinasesTumor Suppressor ProteinsCell DifferentiationCell BiologyNewbornEmbryonic stem cellNeural stem cellMegalencephalyCell biologynervous system diseasesNeuroepithelial cellmedicine.anatomical_structureAnimals NewbornImmunologyGene TargetingMutationmTORMolecular MedicineTSC1TSC2Signal Transduction
researchProduct