通过ERα增加STING的表达,在慢性子宫内膜炎期间对抗LCN2下调
Min Chu1, Shunzhi He1, Huishan Zhao1
1Reproductive Medicine Center, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, No. 20 Yuhuangding Estern Road, Yantai 264000, People's Republic of China.
Journal of reproductive immunology
|November 12, 2023
概括
与慢性子宫内膜炎相关的不孕症涉及改变的抗微生物 (AMP) 和雌激素受体α (ERα). 这项研究表明,ERα调节STING和LCN2的表达,影响粘膜免疫力.
科学领域:
- 生殖免疫学 生殖免疫学
- 微生物的病原发生.
- 这是天生的免疫力.
背景情况:
- 慢性子宫内膜炎与不孕症有关,涉及子宫内膜微生物群感染.
- 防御素,雌激素和雌激素受体在慢性子宫内膜炎中的作用尚未完全理解.
- 抗微生物 (AMP) 在膜对病原体的防御中至关重要.
研究的目的:
- 研究慢性子宫内膜炎中特定AMP (hNP-1,hBD-1-4,LCN2) 和雌激素/雌激素受体的表达.
- 探索STING通路在慢性子宫内膜炎中的参与.
- 在这种情况下,阐明雌激素受体α (ERα),STING和LCN2之间的关系.
主要方法:
- 从患有和没有慢性子宫内膜炎的妇女身上分析人类子宫内膜组织.
- 对AMP,雌激素和ERα表达的定量评估.
- 药理上抑制ERα (raloxifene) 和STING (H-151) 以研究途径调节.
主要成果:
- 在子宫内膜炎组织中,hBD-1和LCN2的调节下降,而hBD-2,hBD-3,hBD-4,hNP-1,雌激素和ERα的调节上升.
- 通过ERα抑制调节了STING表达和酸化.
- 抑制ERα和STING显著降低了LCN2的表达.
结论:
- 雌激素受体α (ERα) 在慢性子宫内膜炎中被上调,并起到调节STING表达的作用.
- ERα通过STING途径影响LCN2抗微生物的表达,影响粘膜免疫力.
- 这些发现表明,通过向ERα-STING-LCN2轴,可以针对慢性子宫内膜炎的新型治疗点.
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