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通过调节热和JAK2/STAT3信号通路,LILRB4 Knockdown 抑制了大动脉剖析的发展

Jianxian Xiong^1,2, Jiayuan Ling³, Jie Yan⁴

¹Department of Cardiovascular Surgery, First Affiliated Hospital of Gannan Medical University, No. 23, Qingnian Road, Zhanggong District, Ganzhou City, 341000, Jiangxi Province, China.

Scientific reports

|July 6, 2024

概括

白细胞免疫球蛋白样受体B4 (LILRB4) 敲除通过抑制热和JAK2/STAT3通路,提高了生存率并减少了大动脉剖析 (AD). 这为AD提供了潜在的治疗点.

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
分子医学是分子医学.

背景情况:

大动脉解剖 (AD) 是一种严重的疾病,死亡率高,药物治疗有限.
之前的研究表明,白细胞免疫球蛋白样受体B4 (LILRB4) 敲除促进AD细胞亡和收缩表型.
在AD病变发生过程中LILRB4的确切作用及其分子机制尚未完全阐明.

研究的目的:

在大动脉剖析的动物模型中研究LILRB4的作用.
阐明LILRB4在AD中的功能背后的分子机制.
评估在AD中准LILRB4的治疗潜力.

主要方法:

建立了体内 (老鼠) 和体外 (人类大动脉光滑肌细胞) 的大动脉剖析模型.
使用LILRB4淘汰策略和一个JAK2抑制剂 (AG490).
评估了他的病理学变化,烧灭,细胞表型,细胞外矩阵 (ECM) 改造和JAK2 / STAT3信号传递.

主要成果:

在AD中LILRB4的表达很高;它的淘汰增加了存活率,减少了AD发病率,并改善了小鼠的组织病理学.
在AD模型中,LILRB4 Knockdown促进了收缩性表型,稳定了ECM,并抑制了热.
LILRB4 knockdown抑制了JAK2/STAT3信号通路;AG490模仿了对AD细胞的一些抑制作用.

结论:

LILRB4的敲击证明了对大动脉剖析发展的保护作用.
准LILRB4可能是大动脉剖析的新疗法策略.
抑制热和JAK2 / STAT3通路是通过LILRB4敲除在AD中发挥有益作用的关键机制.

关键词:

动脉剖析是一个大动脉剖析.这就是LILRB4的原因.热灭菌的发生.在JAK2/STAT3信号通道.

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