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通过VEGFR2-Cbl-NF-κB信号传导,FAK活动加剧了受阻流媒介动脉样硬化

James M Murphy¹, Duyen Thi Kieu Tran¹, Kyuho Jeong^2,3

¹Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294.

bioRxiv : the preprint server for biology

|December 16, 2024

概括

血流干扰通过激活焦粘附激酶 (FAK) 和血管内皮生长因子受体2 (VEGFR2) 来促进血管炎症. 抑制内皮细胞中的FAK活性可能会减少动脉样硬化中的炎症.

科学领域:

心血管生物学心血管生物学
内皮细胞信号传递
动脉样硬化病原体的产生

背景情况:

动脉样硬化发生在血液流动受损的地方,导致血管炎症.
干扰的流量增加了内皮细胞 (EC) 透性和炎症基因表达.
血管内皮生长因子受体2 (VEGFR2) 在流动诱导的EC炎症中起作用,但其信号通路需要进一步阐明.

研究的目的:

调查焦粘附激酶 (FAK) 在流介导信号中的作用及其与内皮细胞中VEGFR2的联系.
在干扰流动诱导炎症的背景下,阐明连接FAK和VEGFR2的分子机制.

主要方法:

利用细胞培养模型和养西方饮食的Apoe-/-小鼠.
在不同的流量条件下研究了FAK,VEGFR2和NF-κB的激活.
研究了FAK,卡西塔斯B系淋巴瘤 (CBL) 和VEGFR2.2之间的相互作用.

主要成果:

用VEGF进行VEGFR2原始化对于FAK和NF-κB的流动诱导激活至关重要.
FAK激活导致CBL的氨酸酸化,CBL在流动下与VEGFR2相互作用.
Apoe-/-小鼠在阿瑟罗扰乱的流动区域中显示出增加的FAK活性,与ECs上升的表面VEGFR2相关.

结论:

FAK激活是流媒体内皮炎症中VEGFR2信号通路的关键组成部分.
准内皮细胞中的FAK活性可能是缓解动脉样硬化中血管炎症的治疗策略.

关键词:

动脉样硬化是一种动脉样硬化.Cblbl Cblbl Cblbl Cblbl Cblbl Cblbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl Cbl 这是真实的,真实的,真实的.在 NF-κBB 中.在VEGFR2的基础上,VEGFR2 干扰了流动的干扰.

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