Proliferation deficits and gene expression dysregulation in Down's syndrome (Ts1Cje) neural progenitor cells cultured from neurospheres
Identifieur interne : 000126 ( France/Analysis ); précédent : 000125; suivant : 000127Proliferation deficits and gene expression dysregulation in Down's syndrome (Ts1Cje) neural progenitor cells cultured from neurospheres
Auteurs : Randal X. Moldrich [France, Australie] ; Luce Dauphinot [France] ; Julien Laffaire [France] ; Tania Vitalis [France] ; Yann Hérault [France] ; Philip M. Beart [Australie] ; Jean Rossier [France] ; Denis Vivien [France] ; Corinne Gehrig [Suisse] ; Stylianos E. Antonarakis [Suisse] ; Robert Lyle [Suisse] ; Marie-Claude Potier [France]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2009-11-01.
English descriptors
- KwdEn :
Abstract
Down's syndrome neurophenotypes are characterized by mental retardation and a decreased brain volume. To identify whether deficits in proliferation could be responsible for this phenotype, neural progenitor cells were isolated from the developing E14 neocortex of Down's syndrome partial trisomy Ts1Cje mice and euploid (WT) littermates and grown as neurospheres. Ts1Cje neural progenitors proliferated at a slower rate, because of a longer cell cycle, and a greater number of cells were positive for glial fibrillary acidic protein. An increase in cell death was also noted. Gene expression profiles of neural progenitor cells from Ts1Cje and WT showed that 54% of triploid genes had expression ratios (Ts1Cje/WT) significantly greater than the expected diploid gene ratio of 1.0. Some diploid genes associated with proliferation, differentiation, and glial function were dysregulated. Interestingly, proliferation and gene expression dysregulation detected in the Ts1Cje mice did not require overexpression of the chromosome 21 genes amyloid precursor protein (App) and soluble superoxide dismutase 1 (Sod1). © 2009 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.22131
Affiliations:
- Australie, France, Suisse
- Centre-Val de Loire, Région Centre, Île-de-France
- Caen, Orléans, Paris
- Université d'Orléans
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 000C57
- to stream Istex, to step Curation: 000C55
- to stream Istex, to step Checkpoint: 000C87
- to stream Main, to step Merge: 001180
- to stream Main, to step Curation: 001178
- to stream Main, to step Exploration: 001178
- to stream France, to step Extraction: 000126
Links to Exploration step
ISTEX:7872C596FE9257F4EAAB21BEF279D92CDF0103A4Le document en format XML
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<front><div type="abstract" xml:lang="en">Down's syndrome neurophenotypes are characterized by mental retardation and a decreased brain volume. To identify whether deficits in proliferation could be responsible for this phenotype, neural progenitor cells were isolated from the developing E14 neocortex of Down's syndrome partial trisomy Ts1Cje mice and euploid (WT) littermates and grown as neurospheres. Ts1Cje neural progenitors proliferated at a slower rate, because of a longer cell cycle, and a greater number of cells were positive for glial fibrillary acidic protein. An increase in cell death was also noted. Gene expression profiles of neural progenitor cells from Ts1Cje and WT showed that 54% of triploid genes had expression ratios (Ts1Cje/WT) significantly greater than the expected diploid gene ratio of 1.0. Some diploid genes associated with proliferation, differentiation, and glial function were dysregulated. Interestingly, proliferation and gene expression dysregulation detected in the Ts1Cje mice did not require overexpression of the chromosome 21 genes amyloid precursor protein (App) and soluble superoxide dismutase 1 (Sod1). © 2009 Wiley‐Liss, Inc.</div>
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