马拉特1通过miR-101-3p/VEGFA轴调节 trofhoblast 现型
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Wannan Medical College, Wuhu, 241000, China.
Archives of biochemistry and biophysics
|July 12, 2023
概括
在早期发育前症 (ePE) 中,长非编码RNA MALAT1 的水平降低,胎盘组织损害了热囊细胞功能. 通常情况下,MALAT1通过降低miR-101-3p和血管内皮生长因子A (VEGFA) 的调节来促进 trofhoblast 增殖和入侵.
科学领域:
- 生殖生物学 生殖生物学
- 分子遗传学 分子遗传学
- 病理学 病理学 病理学
背景情况:
- 孕前 (PE) 是一种严重的妊娠并发症,与不良的胎盘和异常的子宫螺旋动脉重塑有关.
- 异常的热细胞增殖和亡是PE异常胎盘的关键特征.
研究的目的:
- 为了研究长非编码RNAMALAT1在早期发作的孕前 (ePE) 时的热囊细胞增殖中的作用.
- 阐明MALAT1在调节 trofhoblast 功能的基础分子机制.
主要方法:
- 从ePE和对照患者的胎盘组织中量化MALAT1水平.
- 使用HTR-8/SVneo和JAR细胞进行体外研究,以评估MALAT1对热囊细胞增殖,迁移,入侵和亡的影响.
- 使用敲击,抑制剂,模仿和光酶试验对MALAT1/miR-101-3p/VEGFA轴的研究.
主要成果:
- 在ePE胎盘组织中,MALAT1水平下降,与新生儿出生体重有积极的相关性.
- 马拉特1 knockdown 损害了 trofhoblast 活力,增殖,迁移,入侵和细胞周期进展,同时促进了细胞亡.
- MALAT1的淘汰导致了miR-101-3p的上调和VEGFA的下调;miR-101-3p直接针对MALAT1和VEGFA.
结论:
- 内源性MALAT1通过抑制miR-101-3p和随后的VEGFA来促进 trofhoblast的增殖,迁移和入侵.
- 胎盘组织中MALAT1水平的降低可能会导致早发性孕前的发病.
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