CXCL12 N-terminal end is sufficient to induce chemotaxis and proliferation of neural stem/progenitor cells

Neural stem/progenitor cells (NSC) respond to injury after brain injuries secreting IL-1, IL-6, TNF-alpha, IL-4 and IL-10, as well as chemokine members of the CC and CXC ligand families. CXCL12 is one of the chemokines secreted at an injury site and is known to attract NSC-derived neuroblasts, cells...

Descripción completa

Detalles Bibliográficos
Autores: Filippo, Thais Raquel Martins [UNIFESP], Galindo, Layla Testa [UNIFESP], Barnabé, Gabriela Filoso [UNIFESP], Ariza, Carolina Batista [UNIFESP], Mello, Luiz Eugenio Araujo de Moraes [UNIFESP], Juliano, Maria Aparecida [UNIFESP], Juliano, Luiz [UNIFESP], Porcionatto, Marimélia Aparecida [UNIFESP]
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2013
País:Brasil
Institución:Universidade Federal de São Paulo (UNIFESP)
Repositorio:Repositório Institucional da UNIFESP
Idioma:inglés
OAI Identifier:oai:repositorio.unifesp.br:11600/36666
Acceso en línea:http://dx.doi.org/10.1016/j.scr.2013.06.003
http://repositorio.unifesp.br/handle/11600/36666
Access Level:acceso abierto
Descripción
Sumario:Neural stem/progenitor cells (NSC) respond to injury after brain injuries secreting IL-1, IL-6, TNF-alpha, IL-4 and IL-10, as well as chemokine members of the CC and CXC ligand families. CXCL12 is one of the chemokines secreted at an injury site and is known to attract NSC-derived neuroblasts, cells that express CXCL12 receptor, CXCR4. Activation of CXCR4 by CXCL12 depends on two domains located at the N-terminal of the chemokine. in the present work we aimed to investigate if the N-terminal end of CXCL12, where CXCR4 binding and activation domains are located, was sufficient to induce NSC-derived neuroblast chemotaxis. Our data show that a synthetic peptide analogous to the first 21 amino acids of the N-terminal end of CXCL12, named PepC-C (KPVSLSYRCPCRFFESHIARA), is able to promote chemotaxis of neuroblasts in vivo, and stimulate chemotaxis and proliferation of CXCR4+ cells in vitro, without affecting NSC fate. We also show that PepC-C upregulates CXCL12 expression in vivo and in vitro. We suggest the N-terminal end of CXCL12 is responsible for a positive feedback loop to maintain a gradient of CXCL12 that attracts neuroblasts from the subventricular zone into an injury site. (C) 2013 the Authors. Published by Elsevier B.V. All rights reserved.

Similares en LA Referencia