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Am J Physiol Heart Circ Physiol 277: H1593-H1599, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 4, H1593-H1599, October 1999

Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress

Ying-Li Hu, Song Li, John Y.-J. Shyy, and Shu Chien

Department of Bioengineering and Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, California 92093-0427

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 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.

cell death; endothelial cells


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