IL-17A诱导了膜内皮炎症,并加剧了动脉疾病
Zhao Yang1, Jichao Zhang1, Yuexin Zhu1
1Beijing Anzhen Hospital, Capital Medical University, Beijing, China; Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China.
Biochemical and biophysical research communications
|June 24, 2023
概括
介质素-17A (IL-17A) 信号传递通过增加炎症和纤维化,促进结石性大动脉病 (CAVD). 准IL-17A-IL-17RA通路可能为CAVD提供新的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 翻译医学是一种翻译医学.
背景情况:
- 气性大动脉病 (CAVD) 涉及炎症和纤维气性重塑.
- 干白素-17A (IL-17A) 涉及炎症和纤维状况.
- 之前的研究指出,IL-17A产生细胞和人体化门中的IL-17RA,但其在CAVD病原发生中的作用尚不清楚.
研究的目的:
- 调查IL-17A信号传递在CAVD开始和进展中的作用.
- 探索IL-17A对膜内皮细胞 (VEC) 和相关炎症通路的影响.
主要方法:
- 对公共转录组数据库和人类大动脉膜中的基因表达的分析.
- 在Apoe淘汰赛小鼠中使用5/6切除术开发CAVD的小鼠模型.
- 用IL-17A中和抗体治疗和评估膜化和基因表达.
- 免疫光学,qRT-PCR,RNA测序和细胞计数珠阵列分析在人体门和初级VEC上.
主要成果:
- 在化门中激活IL-17A-IL-17RA信号, IL-17A,IL-17RA和RUNX2表达的增加与化相关.
- 在小鼠模型中,IL-17A中和降低了膜化和RUNX2表达.
- 在VEC中,IL-17A诱导的炎症信号通路,细胞因子/化学因子的产生 (IL-6,IL-1β,CXCL2,CXCL8) 和与纤维化相关的基因 (COL16A1) 表达.
- 在人类大动脉膜的VEC中,IL-17RA被丰富地表达.
结论:
- 升高的IL-17A通过促进VEC激活,炎症和纤维化来促进CAVD.
- 准IL-17A-IL-17RA通路为CAVD提供了一个潜在的治疗策略.
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