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USP22是人类子宫内膜层细胞增殖和决定化所需的,该过程是通过对FoxM1进行二氧化化

Mengqi Zhou¹, Yue Gao², Shujuan Wu¹

¹Reproductive Medical Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China; Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei 430060, China.

Cellular signalling

|June 19, 2024

概括

乌比奎丁特异性蛋白酶22 (USP22) 通过与叉头盒M1 (FoxM1) 相互作用,影响人类子宫内膜层细胞 (HESC) 增殖和脱细胞化. 在复发性植入失败 (RIF) 中,USP22和FoxM1的调控下降,这表明它们在RIF病变发生过程中发挥了作用.

科学领域:

生殖生物学生殖生物学
细胞和分子医学细胞和分子医学
妇科妇科医生妇科

背景情况:

复发性植入失败 (RIF) 仍然是辅助生殖技术 (ART) 的一个挑战.
缺少子宫内膜受容性和异常的人体子宫内膜层细胞 (HESC) 功能是RIF的关键因素.
乌比奎丁特异性蛋白酶22 (USP22) 涉及小鼠子宫内膜层细胞脱细胞化,但其在人体细胞和RIF中的作用尚不清楚.

研究的目的:

调查USP22在人类子宫内膜层细胞 (HESC) 增殖和决定化中的作用.
探索USP22在HESC中与叉头盒M1 (FoxM1) 相关的分子机制.
确定USP22和FoxM1在患有复发性植入失败 (RIF) 的患者子宫内膜中的表达水平.

主要方法:

对临床子宫内膜组织样本的分析.
使用人类子宫内膜层细胞 (HESC) 进行体外研究,以检查USP22和FoxM1的表达和功能.
USP22 在HESC中进行敲击和过度表达实验.
脱化试验评估USP22对FoxM1.1的影响.

主要成果:

在人类子宫内膜的分泌阶段,USP22的表达很高.
USP22的淘汰减少了HESC的扩散和决定,减少了FoxM1的表达;USP22的过度表达产生了相反的效果.
在HESC中,USP22直接使FoxM1脱.
发现USP22和FoxM1都在RIF患者的子宫内膜下调.

结论:

USP22显著影响HESC的扩散和分离,可能是通过其与FoxM1.1的相互作用和分离.
在RIF患者中USP22和FoxM1的下调表明它们参与了复发性植入失败的致病性.
USP22代表了改善RIF中的子宫内膜接受性的潜在治疗标.

关键词:

决心实现二元化叉头盒 M1 叉头盒人体子宫内膜层细胞经常发生的植入失败.乌比基特异性蛋白酶222的使用

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