Tumor necrosis factor-α enhances hypoxia-reoxygenation-mediated apoptosis in cultured human coronary artery endothelial cells:: critical role of protein kinase C
Tumor necrosis factor-α enhances hypoxia-reoxygenation-mediated apoptosis in cultured human coronary artery endothelial cells:: critical role of protein kinase C
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DOI：
10.1016/s0008-6363(98)00342-3
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发表时间：
1999-06-01
影响因子：
10.8
通讯作者：
Mehta, JL
中科院分区：
文献类型：
--
作者：
Li, DY;Yang, BC;Mehta, JL
背景：缺血和缺血时释放的肿瘤坏死因子-α（TNF-α）共同引起心肌组织的凋亡和坏死。由于内皮细胞在决定心脏功能方面可能是至关重要的，因此我们在培养的人冠状动脉内皮细胞（HCAECs）中研究了TNF α和缺氧-复氧之间关于诱导凋亡和潜在信号通路的相互作用。方法与结果：培养HCAEC并暴露于单独缺氧、缺氧-复氧、单独TNF α、TNF α加缺氧-复氧或仅在复氧期间暴露TNF α。通过透射电镜、DNA缺口末端标记和DNA梯状电泳检测细胞凋亡。单纯缺氧可引起培养的HCAECs适度的时间依赖性凋亡，复氧可增加凋亡细胞的数量（P
Background: Ischemia and tumor necrosis factor-alpha (TNF alpha) released during ischemia both cause apoptosis and necrosis of myocardial tissues. Since endothelium may be critically important in determination of cardiac function, we examined the interaction between TNF alpha and hypoxia-reoxygenation with regard to induction of apoptosis and underlying signaling pathway in cultured human coronary artery endothelial cells (HCAECs). Methods and results: HCAECs were cultured and exposed to hypoxia alone, hypoxia-reoxygenation, TNF alpha alone, TNF alpha plus hypoxia-reoxygenation, or TNF alpha only during the period of reoxygenation. Apoptosis was evaluated by transmission electron microscopy, DNA nick-end labeling and DNA laddering. Hypoxia alone caused modest time-dependent apoptosis of cultured HCAECs, and reoxygenation increased the number of apoptotic cells (P