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










Base de dados
Intervalo de ano de publicação
1.
Exp Mol Pathol ; 117: 104525, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-32888957

RESUMO

Cerebral ischemia-reperfusion (CIR) can regulate multiple transcription factors to enhance or attenuate injury. Nucleotide-binding oligomerization domain protein 1 (NOD1) has been reported to be involved in autophagy and endoplasmic reticulum (ER) stress. Moreover, autophagy and ER stress play important roles in CIR injury. Hence, the function of NOD1 in CIR injury was explored in this study. Primary rat cortical neurons were treated with oxygen-glucose deprivation and reperfusion (OGD/R) in vitro. NOD1 level was measured using immunofluorescence, real-time quantitative PCR and western blotting and its ubiquitination using co-immunoprecipitation. Results showed that OGD/R up-regulated NOD1 level but inhibited NOD1 ubiquitination. Then the effect of NOD1 on OGD/R-induced changes in cell viability, apoptosis, autophagy and ER stress was evaluated by methyl thiazolyl tetrazolium assay, lactate dehydrogenase release, Hoechst staining, detection of autophagy and ER stress-related proteins using western blotting and infection with GFP-LC3 lentiviruses. OGD/R decreased cell viability and increased cell apoptosis. NOD1 up-regulation promoted these changes, but NOD1 down-regulation reversed these changes. Moreover, OGD/R triggered autophagy and ER stress and NOD1 silencing reversed OGD/R-induced changes in autophagy and ER stress. To validate the role of autophagy in OGD/R injury, autophagy inducer rapamycin was used. Rapamycin promoted OGD/R-induced decrease in cell viability and counteracted NOD1 silencing-induced increase in cell viability. In addition, ER stress inducer tunicamycin was used to investigate the relationship between ER stress and autophagy. Tunicamycin promoted OGD/R-induced decrease in cell viability and reversed NOD1 silencing-induced increase in cell viability. Tunicamycin also enhanced OGD/R-induced autophagy and reversed NOD1 silencing-induced inhibition in autophagy. The results indicated that NOD1 promoted OGD/R injury in cortical neurons through activating ER stress-mediated autophagy. This study provides new insights for the target of CIR injury treatment.


Assuntos
Isquemia Encefálica/genética , Estresse do Retículo Endoplasmático/genética , Proteína Adaptadora de Sinalização NOD1/genética , Traumatismo por Reperfusão/genética , Animais , Apoptose/genética , Autofagia/genética , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Sobrevivência Celular/genética , Córtex Cerebelar/metabolismo , Córtex Cerebelar/patologia , Glucose/metabolismo , Humanos , Neurônios/metabolismo , Neurônios/patologia , Oxigênio/metabolismo , Ratos , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...