在羊群中,LPS通过抑制STAT1酸化来破坏子宫内膜受体性
Xing Fan1, Jinzi Wei1, Yu Guo1
1College of Animal Science and Technology, Northeast Agricultural University, Harbin 150038, China.
International journal of molecular sciences
|January 8, 2025
概括
来自格拉姆阴性细菌的脂聚糖 (LPS) 通过JAK2/STAT1通路破坏子宫内膜受容性,从而损害绵羊胚胎的植入. 这导致受孕率降低和怀孕失败.
科学领域:
- 生殖生物学 生殖生物学
- 免疫学 免疫学 免疫学
- 遗传学 是一个遗传学.
背景情况:
- 子宫感染会对反动物的繁殖效率产生负面影响.
- 格拉姆阴性细菌感染,特别是脂聚糖 (LPS) 暴露,导致生殖功能障碍,包括植入失败和受孕率降低.
研究的目的:
- 调查LPS输液在关键胚胎植入期期间对羊的子宫内膜接受度的影响.
- 阐明分子机制,特别是JAK2 / STAT1通路,涉及LPS诱导的子宫内膜受体性损伤.
主要方法:
- 在12日,16日和20日对孕羊进行体内LPS输注.
- 用激素和LPS进行羊子宫内膜上皮细胞的体外治疗.
- 与植入,前列腺素和JAK/STAT通路相关的基因和蛋白质表达的分析.
- 使用p-STAT1抑制剂 (fludarabine) 的验证.
主要成果:
- 输入LPS改变了前列腺素,粘附因子,关键植入基因 (HOXA10,HOXA11,LIF) 和延长基因 (ISG15,RSAD2,CXCL10) 的表达.
- LPS显著降低了p-STAT1和增加了IRF9蛋白水平,表明了JAK2/STAT1通路的参与.
- 实验室模型证实,LPS和p-STAT1抑制降低了前列腺素合成,并抑制了关键植入基因表达.
结论:
- 妊娠12日,16日和20日的LPS输液会损害绵羊的子宫内膜受体.
- JAK2/STAT1通路是羊中LPS诱导的生殖衰竭的关键调解者.
- 准JAK2/STAT1通路可能为LPS相关的怀孕流产提供治疗策略.
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