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PDCD4缺乏改善了4 - 乙烯基二氧化物诱导的小鼠早产卵巢衰竭

Jie Zhang¹, Mengzhen Qin², Chunyu Kao³

¹The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.

Reproductive biomedicine online

|February 7, 2024

概括

编程细胞死亡4 (PDCD4) 在早产卵巢衰竭 (POI) 中被上调. 在小鼠中减少PDCD4通过影响PI3K-AKT-Bcl2/Bax通路改善了卵巢功能,这表明POI的治疗标.

科学领域:

生殖生物学生殖生物学
分子内分泌学分子内分泌学
细胞死亡机制细胞死亡机制

背景情况:

过早卵巢衰竭 (POI) 是一种影响生育年龄妇女的衰弱性疾病.
在POI病原体的基础上的分子机制仍然不完全理解.
编程细胞死亡4 (PDCD4) 是一种已知的瘤抑制剂和细胞亡的调节剂.

研究的目的:

调查PDCD4在早产卵巢缺陷 (POI) 的发展和进展中的作用.
探索针对PDCD4进行POI治疗干预的潜力.

主要方法:

使用4-乙烯基二氧化物 (VCD) 生成PDCD4基因淘汰 (PDCD4-/-) 和POI小鼠模型.
在体外和体内研究中构建PDCD4过度表达的腺病毒.
在人类和小鼠卵巢颗粒细胞中量化PDCD4表达.
评估卵巢功能标志物 (抗米勒尔激素,雌激素,卵泡数) 和信号通路 (PI3K-AKT-Bcl2/Bax).

主要成果:

在人类POI患者和VCD诱导的POI小鼠的卵巢颗粒细胞中,PDCD4表达显著升高.
在POI小鼠中,PDCD4淘汰导致抗穆勒尔激素,雌激素和发育毛囊的显著增加.
确定PI3K-AKT信号通路和Bcl2/Bax比为PDCD4对POI影响的关键调解器.

结论:

在POI病理学中,PDCD4的表达和调节起着至关重要的作用.
调节PDCD4水平会影响卵巢功能和卵泡发育.
针对PI3K-AKT-Bcl2/Bax通路与PDCD4结合,为POI提供了一个潜在的治疗策略.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.在POI,PDCD4 这是一个VCD,VCD,VCD.

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