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降低NSD2通过重新编程H3K36me2损害了人类子宫内膜中细胞的增殖

Chuan-Mei Qin^1,2,3, Xiao-Wei Wei⁴, Jia-Yi Wu^1,2,3

¹The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Reproduction (Cambridge, England)

|January 18, 2024

概括

核受体结合SET域蛋白2 (NSD2) 降低,通过改变MCM7基因促进者的H3K36me2甲基化,损害了在复发性植入失败 (RIF) 中的子宫内膜层细胞增殖.

科学领域:

生殖生物学生殖生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
细胞增殖细胞的增殖

背景情况:

反复植入失败 (RIF) 在辅助生殖技术中是一个重大挑战,原因是对分子机制的理解不足.
损伤的人体子宫内膜层细胞 (HESC) 增殖破坏子宫内膜-卵巢循环,导致胚胎-子宫内膜异步.
组织素甲基化酶在调节HESC增殖中的作用在很大程度上是未知的.

研究的目的:

调查基因组甲基转移酶NSD2和H3K36me2甲基化在RIF患者观察到的子宫内膜增殖缺陷中的作用.
阐明在RIF中受损的HESC增殖背后的表观遗传机制.

主要方法:

在RIF患者子宫内膜中量化NSD2水平和H3K36me2.
在HESC中进行NSD2淘汰,然后进行全球H3K36me2评估.
转录和RNA测序分析以确定受影响的基因和途径.
使用CUT&Tag测序和ChIP-qPCR来确定H3K36me2在MCM7促进体的结合.

主要成果:

在RIF患者的生殖期子宫内膜中,NSD2和H3K36me2水平显著下降.
在HESC中抑制NSD2会损害细胞增殖,并减少H3K36me2.2.
细胞循环相关的基因,包括MCM7,在RIF子宫内膜和NSD2敲击HESC中被下调.
NSD2的淘汰减少了H3K36me2与MCM7促进体的结合,导致MCM7表达的减少.

结论:

降低NSD2通过H3K36me2甲基化在MCM7促进体上的表观遗传重编程,损害了RIF患者的增殖期子宫内膜层细胞增殖.
这项研究揭示了一种新的表观基因组规模机制,有助于RIF病理生理学.
准NSD2或H3K36me2通路可能为RIF提供治疗策略.

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