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外体YB-1通过MALAT1/miR-211-5p/FOXO轴促进卵巢的恢复

Mengxue Zhang^1,2, Jie Xing^1,3, Shijie Zhao^1,4

¹Reproductive Center, The Fourth Affiliated Hospital of Jiangsu University, 20 Zhengdong Road, Zhenjiang, Jiangsu, 212001, People's Republic of China.

Cell biology and toxicology

|May 3, 2024

概括

介酶干细胞衍生的细胞外囊泡通过输送YB-1蛋白来恢复过早卵巢衰竭 (POF) 的卵巢功能. 这种YB-1蛋白调节MALAT1/miR-211-5p/FOXO3通路,改善粒粉细胞功能和卵巢健康.

科学领域:

生殖生物学生殖生物学
干细胞生物学干细胞生物学
分子医学是分子医学.

背景情况:

过早的卵巢衰竭 (POF) 在40岁以下的女性中导致不孕.
介细胞干细胞衍生小细胞外囊 (MSCs-sEVs) 显示出对POF治疗的前景.
在POF中MSCs-sEVs的关键媒介和机制仍然不清楚.

研究的目的:

确定MSCs-sEV中负责恢复POF中的卵巢功能的关键介质.
阐明MSCs-sEVs发挥治疗作用的潜在分子机制.
研究YB-1蛋白在POF中的作用及其作为治疗点的潜力.

主要方法:

建立了POF的体外 (H2O2) 和体内 (CTX) 模型.
移植骨髓MSCs衍生的sEVs (BMSCs-sEVs) 进入POF大鼠模型.
利用了YB-1的耗尽,并分析了MALAT1/miR-211-5p/FOXO3轴.
在POF患者的血清和粒状细胞 (GCs) 中评估了YB-1水平.

主要成果:

在POF模型和患者中,YB-1蛋白的下调,与GC衰老相关.
在POF大鼠中,BMSCs-sEVs移植上调了YB-1,减弱了GC衰老,并改善了卵巢功能.
YB-1 枯竭逆转了 BMSCs-sEVs 的治疗效果.
YB-1稳定了MALAT1,它充当了miR-211-5p的ceRNA,增加了FOXO3水平并修复了卵巢功能.

结论:

YB-1蛋白是BMSCs-sEVs在治疗POF时提供的关键调解剂.
治疗机制涉及YB-1介导的MALAT1/miR-211-5p/FOXO3轴的调节.
这一途径为管理早产卵巢衰竭提供了潜在的治疗标.

关键词:

马拉特语马拉特语在POF POF中.YB-1 是一个YB-1.sEVs 的使用情况.

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