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转移相关的肺腺癌转录1 丸中的过度表达通过抑制ETS变异转录因子5促成异常非阻塞性精

Lei Wei¹, Zonggang Feng¹, Qian Dou¹

¹Reproductive medical center of The Second Affiliated Hospital of Zhengzhou University, No. 2 Jingba Road, Zhengzhou, Henan, 450014, China.

Molecular biomedicine

|December 16, 2024

概括

转移相关的肺腺癌转录1 (MALAT1) 在异常非阻塞性精症 (iNOA) 中过度表达,抑制ETV5并导致精子干细胞的亡,导致男性不育.

科学领域:

生殖生物学生殖生物学
分子遗传学分子遗传学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

转移相关的肺腺癌转录1 (MALAT1) 是一个长的非编码RNA,涉及各种细胞功能.
异形非阻塞性精子缺血症 (iNOA) 是男性不孕症的主要原因,其潜在的分子机制往往不清楚.
MALAT1在精子生成中的作用及其对iNOA病原体的潜在贡献需要研究.

研究的目的:

阐明MALAT1失调导致iNOA病变的机制.
与对照组相比,分析iNOA患者的MALAT1表达水平.
研究MALAT1过度表达对人类精子干细胞 (SSC) 和塞尔托利细胞的功能影响.

主要方法:

在患者队列中对MALAT1的基因表达分析 (阻塞性亚精细菌与iNOA).
在初级人类SSC和塞尔托利细胞中对MALAT1的过度表达研究.
染色体免疫沉定量PCR (ChIP-qPCR) 来评估ETV5促进体中的表观遗传修饰 (DNA甲基化,H3K27me3,H3K27Ac).

主要成果:

在iNOA患者的丸中,MALAT1显著过度表达.
马拉特1水平与几个与精子发生有关的基因有负相关.
在SSC中MALAT1的过度表达抑制了增殖,诱导了亡,并通过ETV5促进体的H3K27三甲基化抑制了ETS变异转录因子5 (ETV5) 表达.
塞尔托利细胞中MALAT1过度表达会损害它们的功能.

结论:

过度表达MALAT1是iNOA发病的一个关键因素.
通过MALAT1降低ETV5表达和诱导SSC中的亡,有助于iNOA.
马拉特1失调影响SSC和塞尔托利细胞,影响男性生育能力.

关键词:

异常非阻塞性阿佐精子症.长的非编码RNA是什么?马拉特语马拉特语马拉特语精子发生是精子生成.精子干细胞是精子干细胞.

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