Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis.
J Neuroimmunol
; 382: 578152, 2023 09 15.
Article
em En
| MEDLINE
| ID: mdl-37454525
ABSTRACT
The c-Jun amino terminal kinases (JNKs) regulate transcription, and studies suggest they contribute to neuropathology in the EAE model of MS. To examine the role of the JNK3 isoform, we compared EAE in JNK3 null mice to wild type (WT) littermates. Although disease severity was similar in female mice, in male JNK3 null mice the day of onset and time to reach 100% incidence occurred sooner, and disease severity was increased. While glial activation in spinal cord was similar, white matter lesions were increased in JNK3 null mice. These results suggest JNK3 normally limits EAE disease in a sex-dependent manner.
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MEDLINE
Assunto principal:
Proteína Quinase 10 Ativada por Mitógeno
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Esclerose Múltipla
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article