Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress
Sustained JNK activation induces endothelial apoptosis: studies with colchicine and shear stress
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DOI：
10.1152/ajpheart.1999.277.4.h1593
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发表时间：
1999-10-01
影响因子：
4.8
通讯作者：
Chien, S
中科院分区：
文献类型：
--
作者：
Hu, YL;Li, S;Chien, S
DNA梯形和TdT介导的dUTP缺口末端标记荧光染色证明，用10(-7)-10(-5) M秋水仙碱处理牛主动脉内皮细胞，微管破裂导致细胞凋亡。秋水仙碱处理还诱导 c-Jun NH2 末端激酶 (JNK) 持续激活，持续时间大于或等于 12 小时。使用负干扰突变体 JNK(K-R) 阻断 JNK 活性可显着减少秋水仙碱诱导的细胞凋亡。牛主动脉内皮细胞暴露于层流剪切应力 (12 dyn/cm(2)) 会导致短暂的 (
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 greater than or equal to 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 (