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

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...

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Published in:American journal of physiology. Heart and circulatory physiology 1999-10, Vol.277 (4), p.H1593-H1599
Main Authors: Hu, Ying-Li, Li, Song, Shyy, John Y.-J, Chien, Shu
Format: Article
Language:English
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Summary: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 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 (
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.1999.277.4.H1593