Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Más filtros

Banco de datos
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Cell Rep ; 42(11): 113368, 2023 11 28.
Artículo en Inglés | MEDLINE | ID: mdl-37917581

RESUMEN

Ischemic brain injury is a severe medical condition with high incidences in elderly people without effective treatment for the resulting neural damages. Using a unilateral mouse stroke model, we analyze single-cell transcriptomes of ipsilateral and contralateral cortical penumbra regions to objectively reveal molecular events with single-cell resolution at 4 h and 1, 3, and 7 days post-injury. Here, we report that neurons are among the first cells that sense the lack of blood supplies by elevated expression of CCAAT/enhancer-binding protein ß (C/EBPß). To our surprise, the canonical inflammatory cytokine gene targets for C/EBPß, including interleukin-1ß (IL-1ß) and tumor necrosis factor α (TNF-α), are subsequently induced also in neuronal cells. Neuronal-specific silencing of C/EBPß or IL-1ß and TNF-α substantially alleviates downstream inflammatory injury responses and is profoundly neural protective. Taken together, our findings reveal a neuronal inflammatory mechanism underlying early pathological triggers of ischemic brain injury.


Asunto(s)
Lesiones Encefálicas , Accidente Cerebrovascular , Humanos , Ratones , Animales , Anciano , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismo , Regulación de la Expresión Génica , Neuronas/metabolismo , Accidente Cerebrovascular/genética , Accidente Cerebrovascular/metabolismo , Modelos Animales de Enfermedad , Lesiones Encefálicas/metabolismo , Proteína beta Potenciadora de Unión a CCAAT/metabolismo
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA