Neuroprotection from stroke in the absence of MHCI or PirB.
Neuron
; 73(6): 1100-7, 2012 Mar 22.
Article
em En
| MEDLINE
| ID: mdl-22445338
ABSTRACT
Recovery from stroke engages mechanisms of neural plasticity. Here we examine a role for MHC class I (MHCI) H2-Kb and H2-Db, as well as PirB receptor. These molecules restrict synaptic plasticity and motor learning in the healthy brain. Stroke elevates neuronal expression not only of H2-Kb and H2-Db, but also of PirB and downstream signaling. KbDb knockout (KO) or PirB KO mice have smaller infarcts and enhanced motor recovery. KO hippocampal organotypic slices, which lack an intact peripheral immune response, have less cell death after in vitro ischemia. In PirB KO mice, corticospinal projections from the motor cortex are enhanced, and the reactive astrocytic response is dampened after MCAO. Thus, molecules that function in the immune system act not only to limit synaptic plasticity in healthy neurons, but also to exacerbate brain injury after ischemia. These results suggest therapies for stroke by targeting MHCI and PirB.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Receptores Imunológicos
/
Antígenos de Histocompatibilidade Classe I
/
Regulação da Expressão Gênica
/
Recuperação de Função Fisiológica
/
Infarto da Artéria Cerebral Média
Limite:
Animals
Idioma:
En
Revista:
Neuron
Ano de publicação:
2012
Tipo de documento:
Article