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CTRP6通过PPAR-γ/NF-κB通路调节M1巨细胞的两极分化,并在重复性自发性流产中重新编程糖解

Sisi Yan¹, Jinli Ding¹, Zehao Wang¹

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

International immunopharmacology

|September 11, 2023

概括

C1q/瘤亡因子相关蛋白6 (CTRP6) 影响巨细胞两极分化和糖解,影响复发性自发性流产 (RSA). 抑制CTRP6或PPAR-γ在预防胚胎损失方面显示出有前途.

科学领域:

免疫学免疫学免疫学
生殖生物学生殖生物学
代谢过程中的代谢.

背景情况:

异常的果性巨细胞极化与复发性自发性流产 (RSA) 有关.
已知C1q/瘤坏死因子相关蛋白6 (CTRP6) 在炎症和新陈代谢中起作用,但其在RSA中的功能尚不清楚.
在RSA期间了解CTRP6在巨细胞功能中的作用对于开发新疗法至关重要.

研究的目的:

在RSA的背景下,研究CTRP6对巨细胞极化和糖解的调节作用.
阐明涉及CTRP6在RSA病变发生过程中的潜在分子机制.
评估向CTRP6或相关途径的治疗潜力.

主要方法:

叶组织的双免疫光分析,以将CTRP6表达与M1巨细胞标记物相关联 (CD86).
在体外实验中评估CTRP6对巨细胞激活和糖解的影响.
使用动物模型进行体内研究,以评估CTRP6操纵和PPAR-γ激素对胚胎吸收的影响.

主要成果:

在叶组织中,CTRP6表达与M1巨标记物CD86正相关.
通过PPAR-γ/NF-κB通路,CTRP6促进了M1巨细胞的激活,并改变了巨细胞的糖解.
制CTRP6或使用PPAR-γ激动剂 (GW1929) 抑制了M1极化,并在体内挽救了胚胎吸收.

结论:

在RSA期间,CTRP6在调节巨细胞极化和糖解方面发挥着重要作用.
PPAR-γ/NF-κB通路参与了在RSA中CTRP6-介导的巨细胞转化.
针对CTRP6或PPAR-γ是一个潜在的治疗策略,用于复发性自发性流产.

关键词:

在CTRP6中使用.葡萄糖溶解是什么? 葡萄糖溶解巨细胞的两极分化经常发生的自发性流产.

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