Glucocorticoid suppresses BDNF-stimulated MAPK/ERK pathway via inhibiting interaction of Shp2 with TrkB.
FEBS Lett
; 585(20): 3224-8, 2011 Oct 20.
Article
en En
| MEDLINE
| ID: mdl-21946312
ABSTRACT
Increased glucocorticoids (GCs) have been implicated in the pathophysiology of depressive disorder. We previously found that dexamethasone (DEX, a synthetic GC) repressed brain-derived neurotrophic factor (BDNF)-induced synaptic proteins via suppressing extracellular signal-regulated protein kinase (ERK) signaling. Here, we investigated the possible involvement of Src homology-2 domain-containing phosphatase2 (Shp2), an ERK signaling mediator. We found that DEX suppressed Shp2 interaction with TrkB, a receptor for BDNF, in cultured cortical neurons. NSC87877, a Shp2 inhibitor, mimicked DEX, and Shp2 overexpression reversed the effect of DEX, suggesting that GCs suppress ERK signaling through inhibiting the interaction of Shp2 with TrkB.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Dexametasona
/
Factor Neurotrófico Derivado del Encéfalo
/
Receptor trkB
/
Sistema de Señalización de MAP Quinasas
/
Proteína Tirosina Fosfatasa no Receptora Tipo 11
/
Glucocorticoides
/
Neuronas
Límite:
Animals
Idioma:
En
Revista:
FEBS Lett
Año:
2011
Tipo del documento:
Article
País de afiliación:
Japón