热引起的胎儿-母体界面的病理生理和代谢变化,导致早产的发生.
Isidore Mushimiyimana1, Lauren Richardson1, Thomas D Horvath2,3,4,5
1Department of Obstetrics & Gynecology, Division of Basic Science and Translational Research, The University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
概括
全球气温上升与早产风险 (PTB) 有关. 热应激会损害母体和胎儿细胞,导致线粒体功能障碍,氧化应激和炎症,可能导致PTB.
科学领域:
- 生殖生物学 生殖生物学
- 环境健康 环境健康
- 细胞生理学 细胞生理学
背景情况:
- 全球气温上升是与早产 (PTB) 相关的日益关注的问题.
- 对热的病理生理机制的有限理解阻碍了对PTB的临床干预.
研究的目的:
- 为了检查胎儿与母亲接口 (FMis) 的热引起的病理生理和代谢变化.
- 探索这些变化在PTB病理生理学的机制性影响.
主要方法:
- 使用2D体外热暴露模型 (39°C) 与母乳乳细胞 (DECs) 和胎儿乳房上皮细胞 (AECs).
- 评估了线粒体功能,氧化压力 (谷氨),压力信号 (p38MAPK,NF-κB),衰老和炎症 (细胞因子).
- 采用有针对性的代谢学来评估热量诱导的代谢变化.
主要成果:
- 在两种细胞类型中,热应激诱导了线粒体功能障碍 (减少ATP,改变HSPD1,ATP5F1,VDAC1表达) 和氧化应激 (减少GSH).
- 热暴露引发了DNA损伤,p38MAPK激活,衰老和炎症性细胞因子 (IL-6,GM-CSF) 的增加,这表明与衰老相关的分泌表型.
- 代谢分析揭示了能量,氨基酸,表观遗传和免疫相关途径的显著热引起的变化,具有重叠和细胞类型特定的反应.
结论:
- 孕产妇和胎儿的细胞对热应激敏感,表现出不同的病理生物学和代谢干扰.
- 这些发现提供了关于胎儿与母亲界面的热感应细胞反应的见解,有助于对PTB的理解.
- 未来的集成多种FMi细胞类型的模型可以识别用于PTB预测的热相关生物标志物.
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