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Cited by 309

The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.

Generation of an environmental niche for neural stem cell development by the extracellular matrix molecule tenascin C

Garcion, Emmanuel, Halilagic, Aida, Faissner, Andreas, ffrench-Constant, Charles·2004·Development
DOI 10.1242/dev.01202
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Abstract

Stem cells in the embryonic mammalian CNS are initially responsive to fibroblast growth factor 2 (FGF2). They then undergo a developmental programme in which they acquire epidermal growth factor (EGF) responsiveness, switch from the production of neuronal to glial precursors and become localized in specialized germinal zones such as the subventricular zone (SVZ). Here we show that extracellular matrix molecules act as regulators of this programme. Tenascin C is highly expressed in the SVZ, and transgenic mice lacking tenascin C show delayed acquisition of the EGF receptor. This results from alterations in the response of the stem cells to the growth factors FGF2 and bone morphogenic protein 4 (BMP4), which normally promote and inhibit acquisition of the EGF receptor, respectively. Tenascin C-deficient mice also have altered numbers of CNS stem cells and these stem cells have an increased probability of generating neurones when grown in cell culture. We conclude that tenascin C contributes to the generation of a stem cell `niche' within the SVZ, acting to orchestrate growth factor signalling so as to accelerate neural stem cell development.

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Metadata

Authors
Garcion, E., Halilagic, A., Faissner, A., & ffrench-Constant, C.
Venue
Development
Publisher
The Company of Biologists
Published
2004-07-15
Volume
131
Issue
14
Pages
3423-3432
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
DOI
10.1242/dev.01202
OpenAlex
W2093885717
Cited by
309
References
67
FWCI
4.67
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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