Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells
Oscillatory Shear Stress Induces Oxidative Stress via TLR4 Activation in Endothelial Cells
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振荡剪切应力通过内皮细胞中的 TLR4 激活诱导氧化应激
DOI：
10.1155/2019/7162976
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发表时间：
2019-06
影响因子：
4.6
通讯作者：
Zhang Junjie
中科院分区：
文献类型：
--
作者：
Wang Zhimei;Wang Feng;Kong Xiangquan;Gao Xiaofei;Gu Yue;Zhang Junjie
背景振荡剪切应力（Oscillatory shear stress，OSS）可破坏内皮细胞的稳态，促进氧化应激，导致动脉粥样硬化。在动脉粥样硬化病变中，Toll样受体4（TLR4）高度表达。然而，TLR4调节OSS后氧化变化和细胞信号转导的分子机制尚未确定。方法和结果颈动脉缩窄术（CAC）和平行板流动室被用来调节剪切应力。结果表明，OSS显著增加了氧化负荷，这部分是由于TLR4激活。OSS激活内皮细胞中的NOX2，对NOX1和NOX4无明显影响。OSS可使caveolin-1磷酸化，促进其与内皮型一氧化氮合酶（eNOS）结合，导致eNOS失活。TLR4抑制恢复了OSS暴露细胞中一氧化氮（NO）和超氧化物歧化酶（SOD）的水平。结论TLR4通过激活NOX2和抑制eNOS调节OSS诱导的氧化应激。
Background Oscillatory shear stress (OSS) disrupts endothelial homeostasis and promotes oxidative stress, which can lead to atherosclerosis. In atherosclerotic lesions, Toll-like receptor 4 (TLR4) is highly expressed. However, the molecular mechanism by which TLR4 modulates oxidative changes and the cell signaling transudation upon OSS is yet to be determined. Methods and Results Carotid artery constriction (CAC) surgery and a parallel-plate flow chamber were used to modulate shear stress. The results showed that OSS significantly increased the oxidative burden, and this was partly due to TLR4 activation. OSS activated NOX2 and had no significant influence to NOX1 or NOX4 in endothelial cells (ECs). OSS phosphorylated caveolin-1, promoted its binding with endothelial nitric oxide synthase (eNOS), and resulted in deactivation of eNOS. TLR4 inhibition restored levels of nitric oxide (NO) and superoxide dismutase (SOD) in OSS-exposed cells. Conclusion TLR4 modulates OSS-induced oxidative stress by activating NOX2 and suppressing eNOS.
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影响因子：
3.3
作者：
Chen Z;D S Oliveira S;Zimnicka AM;Jiang Y;Sharma T;Chen S;Lazarov O;Bonini MG;Haus JM;Minshall RD
通讯作者：
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影响因子：
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4.6
作者：
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影响因子：
4.8
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影响因子：
3.2
作者：
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