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Macrophage stimulating 1-induced inflammation response promotes aortic aneurysm formation through triggering endothelial cells death and activating the NF-κB signaling pathway
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-03-10 , DOI: 10.1080/10799893.2020.1738484
Kai Lu 1 , Jianfei Zhao 1 , Weili Liu 1
Affiliation  

Abstract Aortic aneurysm formation is associated with endothelial cells dysfunction through an undefined mechanism. Macrophage stimulating 1 (Mst1) and NF-κB signaling pathway have been found to be related to inflammation response in endothelial cell damage. The goal of our study is to explore the role of Mst1 in regulating endothelial cell viability with a focus on NF-κB signaling pathway and inflammation response. Endothelial cell viability and death were determined via immunofluorescence and ELISA. Agonist of NF-κB signaling pathway and siRNA against Mst1 were used. The results in our study demonstrated that Mst1 transcription and expression were significantly elevated after exposure to oxidative stress in endothelial cells. Once loss of Mst1 through transfection of siRNA (si-Mst1), endothelial cell viability and survival rate were rapidly increased in response to oxidative stress. In addition, we also found that Mst1 controlled inflammation response and mitochondrial function in endothelial cells. Re-activation of NF-κB signaling pathway was followed by an activation of inflammation response and mitochondrial dysfunction, as evidenced by increased expression of inflammation factors and decreased ATP synthesis. Altogether, our results identify Mst1 as the primary factors responsible for endothelial cells dysfunction in aneurysms formation through inducing inflammation response, endothelial apoptosis, and NF-κB signaling pathway activation.

中文翻译:

巨噬细胞刺激 1 诱导的炎症反应通过触发内皮细胞死亡和激活 NF-κB 信号通路促进主动脉瘤形成

摘要 主动脉瘤形成与内皮细胞功能障碍通过未定义的机制相关。已发现巨噬细胞刺激 1 (Mst1) 和 NF-κB 信号通路与内皮细胞损伤中的炎症反应有关。我们研究的目标是探索 Mst1 在调节内皮细胞活力中的作用,重点是 NF-κB 信号通路和炎症反应。通过免疫荧光和ELISA确定内皮细胞活力和死亡。使用了 NF-κB 信号通路的激动剂和针对 Mst1 的 siRNA。我们的研究结果表明,内皮细胞暴露于氧化应激后,Mst1 的转录和表达显着升高。一旦通过转染siRNA(si-Mst1)丢失Mst1,内皮细胞活力和存活率响应氧化应激而迅速增加。此外,我们还发现 Mst1 控制内皮细胞的炎症反应和线粒体功能。NF-κB 信号通路的重新激活之后是炎症反应和线粒体功能障碍的激活,这可以通过炎症因子表达增加和 ATP 合成减少来证明。总之,我们的结果确定 Mst1 是通过诱导炎症反应、内皮细胞凋亡和 NF-κB 信号通路激活导致动脉瘤形成中内皮细胞功能障碍的主要因素。NF-κB 信号通路的重新激活之后是炎症反应和线粒体功能障碍的激活,这可以通过炎症因子表达增加和 ATP 合成减少来证明。总之,我们的结果确定 Mst1 是通过诱导炎症反应、内皮细胞凋亡和 NF-κB 信号通路激活导致动脉瘤形成中内皮细胞功能障碍的主要因素。NF-κB 信号通路的重新激活之后是炎症反应和线粒体功能障碍的激活,这可以通过炎症因子表达增加和 ATP 合成减少来证明。总之,我们的结果确定 Mst1 是通过诱导炎症反应、内皮细胞凋亡和 NF-κB 信号通路激活导致动脉瘤形成中内皮细胞功能障碍的主要因素。
更新日期:2020-03-10
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