NG2 glia are required for vessel network formation during embryonic development.

Détails

Ressource 1Télécharger: BIB_8107A3117496.P001.pdf (12570.19 [Ko])
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_8107A3117496
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
NG2 glia are required for vessel network formation during embryonic development.
Périodique
Elife
Auteur⸱e⸱s
Minocha S., Valloton D., Brunet I., Eichmann A., Hornung J.P., Lebrand C.
ISSN
2050-084X (Electronic)
ISSN-L
2050-084X
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
4
Pages
e09102
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
The NG2(+) glia, also known as polydendrocytes or oligodendrocyte precursor cells, represent a new entity among glial cell populations in the central nervous system. However, the complete repertoire of their roles is not yet identified. The embryonic NG2(+) glia originate from the Nkx2.1(+) progenitors of the ventral telencephalon. Our analysis unravels that, beginning from E12.5 until E16.5, the NG2(+) glia populate the entire dorsal telencephalon. Interestingly, their appearance temporally coincides with the establishment of blood vessel network in the embryonic brain. NG2(+) glia are closely apposed to developing cerebral vessels by being either positioned at the sprouting tip cells or tethered along the vessel walls. Absence of NG2(+) glia drastically affects the vascular development leading to severe reduction of ramifications and connections by E18.5. By revealing a novel and fundamental role for NG2(+) glia, our study brings new perspectives to mechanisms underlying proper vessels network formation in embryonic brains.
Mots-clé
Animals, Female, Male, Mice, Neovascularization, Physiologic, Neuroglia/physiology, Telencephalon/embryology
Pubmed
Web of science
Open Access
Oui
Création de la notice
17/02/2016 10:17
Dernière modification de la notice
21/11/2022 8:16
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