AHEART October 46/4
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چکیده
Hu, Ying-Li, Song Li, John Y.-J. Shyy, and Shu Chien. Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1593–H1599, 1999.—The disruption of microtubules by treating bovine aortic endothelial cells with 1027–1025 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 NH2-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/cm2) 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.
منابع مشابه
AHEART October 46/4
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