IL-17 induces apoptosis of vascular endothelial cells - A potential mechanism for human acute coronary syndrome
IL-17 induces apoptosis of vascular endothelial cells - A potential mechanism for human acute coronary syndrome
复制标题
DOI：
10.1016/j.clim.2011.07.003
复制
发表时间：
2011-11-01
影响因子：
8.6
通讯作者：
Zhang, Lining
中科院分区：
文献类型：
--
作者：
Zhu, Faliang;Wang, Qun;Zhang, Lining
产生IL-17的Th17细胞参与动脉粥样硬化的发病机制，但其潜在机制仍不清楚。在这项研究中，我们研究了IL-17对人血管内皮细胞的影响，结果表明IL-17诱导血管内皮细胞的细胞死亡，这在引发急性冠脉综合征（ACS）的斑块不稳定中发挥着关键作用。我们发现，与稳定型心绞痛患者或健康个体相比，ACS 患者的循环 Th17 细胞和 IL-17 有所增加； ACS患者血浆IL-6水平升高，TGF-β水平降低，分别与IL-17呈正相关和负相关。重要的是，我们发现IL-17通过激活caspase-3、caspase-9和上调Bax/Bcl-2的比例促进内皮细胞产生von Willebrand因子并诱导内皮细胞凋亡，表明IL-17在血管内皮损伤中的功能是人类ACS发病机制的潜在机制。 (C) 2011 Elsevier Inc. 保留所有权利。
Th17 cells producing IL-17 are involved in the pathogenesis of atherosclerosis, but the underlying mechanisms remain unclear. In this study, we investigated the effects of IL-17 on human vascular endothelial cells and showed that IL-17 induced cell death of the vascular endothelial cells, which played a pivotal role in plaque destabilization triggering acute coronary syndrome (ACS). We showed that circulating Th17 cells and IL-17 increased in patients with ACS compared to the patients with stable angina or health individuals; the plasma levels of IL-6 increased but TGF-beta decreased in ACS patients, exhibiting a positive and negative correlation with that of IL-17, respectively. Importantly, we uncovered that IL-17 promoted the production of von Willebrand factor by endothelial cells and induced endothelial apoptosis by activating caspase-3, caspase-9 and up-regulating the ratio of Bax/Bcl-2, indicating the function of IL-17 in vascular endothelial damage as a potential mechanism for the pathogenesis of human ACS. (C) 2011 Elsevier Inc. All rights reserved.