Alk4/5-dependent tgf-? signaling contributes ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Alk4/5-dependent tgf-? signaling contributes to the crosstalk between neurons and microglia following axonal lesion
Auteur(s) :
Raffo Romero, Antonella [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Arab, Tanina [Auteur]
Van Camp, Christelle [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Lemaire, Quentin [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Wisztorski (admin), Maxence [Auteur]
Franck, Julien [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Aboulouard, Soulaimane [Auteur]
Le Marrec-Croq, Francoise [Auteur]
Sautiere, Pierre-Eric [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Vizioli, Jacopo [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Salzet, Michel [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Lefebvre, Christophe [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Arab, Tanina [Auteur]
Van Camp, Christelle [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Lemaire, Quentin [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Wisztorski (admin), Maxence [Auteur]
Franck, Julien [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Aboulouard, Soulaimane [Auteur]
Le Marrec-Croq, Francoise [Auteur]
Sautiere, Pierre-Eric [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Vizioli, Jacopo [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Salzet, Michel [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Lefebvre, Christophe [Auteur]
Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U1192
Titre de la revue :
Scientific Reports
Nom court de la revue :
Sci Rep
Numéro :
9
Pagination :
6896
Date de publication :
2019-05-03
ISSN :
2045-2322
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Neuronal activity is closely influenced by glia, especially microglia which are the resident immune cells in the central nervous system (CNS). Microglia in medicinal leech are the only cells able to migrate to the injury ...
Lire la suite >Neuronal activity is closely influenced by glia, especially microglia which are the resident immune cells in the central nervous system (CNS). Microglia in medicinal leech are the only cells able to migrate to the injury site within the 24 hours post-lesion. The microglia-neuron interactions constitute an important mechanism as there is neither astrocyte nor oligodendrocyte in the leech CNS. Given that axonal sprouting is impaired when microglia recruitment is inhibited, the crosstalk between microglia and neurons plays a crucial role in neuroprotection. The present results show that neurons and microglia both use ALK4/5 (a type of TGF-beta receptor) signaling in order to maintain mutual exchanges in an adult brain following an axonal injury. Indeed, a TGF-beta family member (nGDF) is immediately released by injured axons contributing to the early recruitment of ALK4/5(+) microglia to the lesion site. Surprisingly, within the following hours, nGDF from microglia activates ALK4/5(+) neurons to maintain a later microglia accumulation in lesion. Taken together, the results demonstrate that ALK4/5 signaling is essential throughout the response to the lesion in the leech CNS and gives a new insight in the understanding of this pathway. This latter is an important signal contributing to a correct sequential mobilization over time of microglia recruitment leading to axon regeneration.Lire moins >
Lire la suite >Neuronal activity is closely influenced by glia, especially microglia which are the resident immune cells in the central nervous system (CNS). Microglia in medicinal leech are the only cells able to migrate to the injury site within the 24 hours post-lesion. The microglia-neuron interactions constitute an important mechanism as there is neither astrocyte nor oligodendrocyte in the leech CNS. Given that axonal sprouting is impaired when microglia recruitment is inhibited, the crosstalk between microglia and neurons plays a crucial role in neuroprotection. The present results show that neurons and microglia both use ALK4/5 (a type of TGF-beta receptor) signaling in order to maintain mutual exchanges in an adult brain following an axonal injury. Indeed, a TGF-beta family member (nGDF) is immediately released by injured axons contributing to the early recruitment of ALK4/5(+) microglia to the lesion site. Surprisingly, within the following hours, nGDF from microglia activates ALK4/5(+) neurons to maintain a later microglia accumulation in lesion. Taken together, the results demonstrate that ALK4/5 signaling is essential throughout the response to the lesion in the leech CNS and gives a new insight in the understanding of this pathway. This latter is an important signal contributing to a correct sequential mobilization over time of microglia recruitment leading to axon regeneration.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
CNRS
INSERM
Université de Lille
INSERM
Université de Lille
Collections :
Date de dépôt :
2022-06-15T13:57:42Z