Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress.
Am J Physiol
; 277(4): H1593-9, 1999 10.
Article
em En
| MEDLINE
| ID: mdl-10516199
ABSTRACT
The disruption of microtubules by treating bovine aortic endothelial cells with 10(-7)-10(-5) M colchicine caused apoptosis, as evidenced by DNA laddering and TdT-mediated dUTP nick end labeling fluorescence staining. Colchicine treatment also induced a sustained activation of c-Jun NH(2)-terminal kinase (JNK) that lasted for >/=12 h. The blockade of JNK activity by using the negative interfering mutant JNK(K-R) markedly decreased the apoptosis induced by colchicine. Exposure of bovine aortic endothelial cells to laminar shear stress (12 dyn/cm(2)) caused a transient (<2 h) activation of JNK, and there was no induction of apoptosis. The sustained activation of JNK may play a significant role in the apoptosis induced by colchicine.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Endotélio Vascular
/
Apoptose
/
Proteínas Quinases Ativadas por Mitógeno
Limite:
Animals
Idioma:
En
Ano de publicação:
1999
Tipo de documento:
Article