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MITA 促进巨细胞的炎症前极化及其与circRNA相关的调节机制在反复流产中

Bowen Liu¹, Jun Liu², Yang Qiu³

¹Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Reproductive Medical Center, Renmin Hospital of Wuhan University, Wuhan 430060, China.

International journal of molecular sciences

|June 10, 2023

概括

MITA (刺痛) 通过增加巨细胞炎症和亡来促进流产. 一种新型的circRNA,cirKIAA0391,通过调节叶巨细胞中的miR-512-5p/MITA通路来加剧这种情况.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
生殖医学生殖医学

背景情况:

米塔 (MITA) 是先天免疫的关键调节者,也是潜在的治疗点.
循环RNA介导网络对于基因调节和疾病至关重要.
MITA及其circRNA机制在反复流产 (RM) 中的作用尚不清楚.

研究的目的:

调查MITA在RM病原发生中的作用.
阐明涉及MITA在RM中的circRNA调节机制.
确定MITA和circKIAA0391对叶巨细胞的影响.

主要方法:

在RM患者中验证了升的M1/M2巨细胞比率.
从RM患者的叶巨细胞中评估了MITA表达.
利用THP-1衍生的巨细胞 (TDM) 来研究MITA的影响.
进行了circRNA测序和生物信息分析.
调查了cirKIAA0391/miR-512-5p/MITA轴的情况.

主要成果:

在RM患者中,决定性M1/M2比率上调.
在RM患者的状巨细胞中,MITA的表达很高.
MITA促进TDM细胞的亡和促炎偏离.
一种新型的circRNA,circKIAA0391,在RM果性巨细胞中过度表达.
circKIAA0391通过miR-512-5p/MITA轴促进TDM细胞亡和促炎性偏离.

结论:

通过影响巨细胞行为,MITA在RM病变发生中发挥着重要作用.
circKIAA0391通过调节miR-512-5p/MITA通路而加剧了RM.
这项研究提供了MITA在RM中的免疫调节功能的见解.

关键词:

这就是MITA MITA.灭症 (apoptosis) 是一种死亡的过程.circKIAA0391 一个圆圈巨细胞的两极分化在 miR-512-5p 中使用.经常发生的流产.

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