Atherosclerosis is a significant cause of mortality and morbidity. Studies suggest that the chemokine receptor CX3CR1 plays a critical role in atherogenesis. Shear stress is an important mechanical force that affects blood vessel function. In this study, we investigated the effect of shear stress on CX3CR1 expression in vascular endothelial cells (VECs). First, cells were exposed to different shear stress and then CX3CR1 mRNA and protein were measured by quantitative RT-PCR and western blot analysis, respectively. CX3CR1 gene silencing was used to analyze the molecular mechanisms underlying shear stress-mediated effects on CX3CR1 expression. CX3CR1 mRNA and protein expression were significantly increased with 4.14 dyne/cm² of shear stress compared with other tested levels of shear stress. We observed a significant increase in CX3CR1 mRNA levels at 2 h and CX3CR1 protein expression at 4 h. CX3CR1-induced VCAM-1 expression in response to low shear stress by activating NF-κB signaling pathway in VECs. Our findings demonstrate that low shear stress increases CX3CR1 expression, which increases VCAM-1 expression due to elevated NF-κB activation. The current study provides evidence of the correlation between shear stress and atherosclerosis mediated by CX3CR1.

中文翻译：

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低剪切应力通过血管内皮细胞中的 NF-κB 通路诱导 VCAM-1，从而上调 CX3CR1 的表达。

动脉粥样硬化是死亡率和发病率的重要原因。研究表明，趋化因子受体 CX3CR1 在动脉粥样硬化形成中起着关键作用。剪切应力是影响血管功能的重要机械力。在这项研究中，我们研究了剪切应力对血管内皮细胞 (VEC) 中 CX3CR1 表达的影响。首先，将细胞暴露于不同的剪切应力，然后分别通过定量 RT-PCR 和蛋白质印迹分析测量 CX3CR1 mRNA 和蛋白质。CX3CR1 基因沉默用于分析剪应力介导的 CX3CR1 表达影响的分子机制。CX3CR1 mRNA 和蛋白表达显着增加 4.14 dyne/cm ²剪切应力与其他测试的剪切应力水平相比。我们观察到 CX3CR1 mRNA 水平在 2 小时显着增加，CX3CR1 蛋白表达在 4 小时显着增加。CX3CR1 通过激活 VEC 中的 NF-κB 信号通路诱导 VCAM-1 表达以响应低剪切应力。我们的研究结果表明，低剪切应力会增加 CX3CR1 的表达，这会因 NF-κB 激活升高而增加 VCAM-1 的表达。目前的研究提供了剪切应力与 CX3CR1 介导的动脉粥样硬化之间相关性的证据。