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通过ADAM17排泄的赤道膜增加了在促炎条件下从人体内皮细胞释放可溶性CD40的释放
Anton Klersy1, Sören Meyer2, Florian Leuschner2
1Department of Cardiovascular Physiology, Heidelberg University, 69120 Heidelberg, Germany.
Cells
|August 11, 2023
概括
CD40基因C等位基因的同胞性与冠状动脉心脏病 (CHD) 有关. ADAM17酶会脱离CD40,增加可溶性CD40 (sCD40),这是一个潜在的CHD生物标志物.
科学领域:
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
- 心血管研究研究心血管研究
背景情况:
- CD40基因的-1T>C多态性 (rs1883832),特别是CC基因型,与冠心病 (CHD) 易感性有关.
- 这种基因型与增加CD40表达和细胞表面脱落有关.
- 众所周知,酶ADAM17可以分裂各种细胞表面蛋白.
研究的目的:
- 为了研究ADAM17介导的CD40分泌和炎症之间的关联.
- 检查ADAM17在具有CC基因型的人体内皮细胞中CD40分泌中的作用.
主要方法:
- 具有CC基因型的人类静脉内皮细胞 (HUVEC) 用可溶性CD40连接体 (sCD40L) 或瘤亡因子-α (TNFα) 进行刺激.
- 使用标准分子生物学技术分析了信使RNA和蛋白质表达水平.
- 在患有心脏病的患者中,使用ELISA测量了可溶性CD40 (sCD40),高灵敏性C反应蛋白 (hs-CRP) 和IL-6 (IL-6) 的血水平.
主要成果:
- 在用CD40L和TNFα刺激后,ADAM17及其调节器iRhom2的表面丰度增加.
- 抑制ADAM17减少了TNFα诱导的sCD40和可溶性血管细胞粘附分子-1的释放,同时增加了表面CD40.
- 在CD40L或TNFα刺激后,ADAM17的抑制导致单细胞化学吸引蛋白-1 (MCP-1) mRNA和蛋白质上调.
- 血sCD40水平与CHD患者的炎症生物标志物hs-CRP和IL-6正相关.
结论:
- 提出了一个机制,即ADAM17从内皮细胞中排出膜结合的CD40,从而增加可溶性CD40 (sCD40) 水平.
- 这种脱落过程可能会限制下游的CD40信号传输.
- 溶性CD40,特别是在CD40基因的CC基因型的个体中,可能作为冠状动脉心脏病的重要生物标志物.
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