由母亲的gal-3缺乏引起的胎儿生长限制与改变的肠-胎盘轴相关
Yiran Xie1, Fangqi Zhao1, Yiru Wang1
1Department of Obstetrics and Fetal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Cell death & disease
|August 8, 2024
概括
孕产妇的加勒-3 (gal-3) 缺乏症会通过肠道微生物组的变化导致胎儿生长受限,影响雌性后代. 父亲的gal-3影响胎盘血管化,突出显示母亲的gal-3.
科学领域:
- 生殖生物学 生殖生物学
- 发育生物学是发展生物学.
- 免疫学 免疫学 免疫学
背景情况:
- 胎儿生长限制 (FGR) 是一种主要的妊娠并发症,具有显著的围产期发病率和死亡率.
- 复杂的FGR病理生理学仍然不完全理解,需要进一步研究潜在的分子机制.
- 加勒-3 (gal-3) 是一种β-galactoside结合蛋白,涉及到关键的怀孕过程,如胎盘和母体血管适应.
研究的目的:
- 调查母体和父体的加勒-3 (gal-3) 在胎儿-胎盘发育和产后结果中的不同作用.
- 阐明母体肠道微生物组和胎盘代谢对-3介导的FGR的贡献.
- 确定-3缺乏对母胎界面的影响及其对后代生长的影响.
主要方法:
- 利用了基因改造的小鼠模型,这些小鼠对母体或父体的甲基素-3有针对性的缺陷.
- 分析了胎儿和胎盘生长参数,胎盘代谢适应 (细胞糖原,Igf2甲基化) 和胎盘血管化.
- 评估母亲的肠道微生物组合及其与胎儿生长结果的相关性.
主要成果:
- 孕产妇的gal-3缺乏导致孕产妇的肠道失调和性别特定的FGR,主要影响女性胎儿和后代.
- 缺乏母体的gal-3与胎盘代谢受损有关,包括降低细胞糖原和Igf2低甲基化.
- 父亲的gal-3缺乏会影响胎盘迷宫血管化,但不会影响胎儿生长轨迹.
结论:
- 产于母体的加勒-3在维持胎儿 - 胎盘发育中发挥着关键作用,可能通过肠 - 胎盘轴.
- 母亲的gal-3以特定性别的方式影响胎盘代谢编程和胎儿生长.
- 盖列-3与母亲和父亲等位基因的差异性贡献突出了其对怀孕结果的复杂调节.
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