Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress
1999 ◽
Vol 277
(4)
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pp. H1593-H1599
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Keyword(s):
The disruption of microtubules by treating bovine aortic endothelial cells with 10−7–10−5M 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.
1996 ◽
Vol 24
(4-5)
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pp. 197-203
1997 ◽
Vol 63
(607)
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pp. 838-845
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1999 ◽
Vol 276
(4)
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pp. C838-C847
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1987 ◽
Vol 7
(3)
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pp. 276-286
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2002 ◽
Vol 282
(4)
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pp. C708-C718
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