在妊娠糖尿病中通过Wnt/β-catenin通路引起的Mucin1诱导的热囊细胞功能障碍
Shuang-Shuang Cui1, Ping Zhang1,2, Lu Sun1
1Department of Gynecology and Obstetrics, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, 510632, China.
Biological research
|August 23, 2023
概括
在妊娠糖尿病 (GDM) 中,高Mucin1 (MUC1) 水平会激活Wnt/β-catenin通路,损害 trofhoblast 葡萄糖吸收并增加亡. 向MUC1显示了GDM治疗的潜力.
科学领域:
- 生殖生物学 生殖生物学
- 内分泌学 在内分泌学.
- 蜂信号传输是如何进行的
背景情况:
- 孕期糖尿病 (GDM) 与胎盘 trofhoblast 功能障碍有关.
- 1 (MUC1) 涉及到热囊细胞功能,包括葡萄糖吸收和亡.
- Wnt/β-catenin信号通路是细胞过程的关键调节器.
研究的目的:
- 为了调查Mucin1 (MUC1) 在热囊细胞葡萄糖吸收和孕期糖尿病 (GDM) 中的亡中的作用.
- 阐明Wnt/β-catenin信号通路在GDM中MUC1-介导的 trofhoblast 功能障碍中的参与.
主要方法:
- 通过GLUT1/GLUT4水平和表达分析了葡萄糖的摄取量.
- 通过Bcl-2,Caspase3表达和流细胞计评估了亡.
- 测量Wnt/β-catenin信号通过西方抹杀在HTR-8/SVneo细胞治疗高葡萄糖,MUC1淘汰,或Wnt/β-catenin抑制剂.
主要成果:
- 在GDM胎盘中,MUC1被上调,与Wnt/β-catenin激活相关,葡萄糖吸收受损,亡增加.
- 在热囊细胞中MUC1的淘汰减少了细胞亡和增加了侵入性.
- 抑制MUC1或抑制Wnt/β-catenin可以逆转高葡萄糖诱导的 trofhoblast 功能障碍.
结论:
- 在GDM中MUC1的升高异常激活了Wnt/β-catenin信号传递,导致热囊细胞功能障碍.
- 这种功能障碍会损害葡萄糖的吸收,并促进GDM患者的胎盘组织的亡.
- MUC1和Wnt/β-catenin信号传输是管理与GDM相关的胎盘并发症的关键目标.
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