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通过MAPK/COX-2通路抑制莱迪格细胞通过MAPK/COX-2通路分泌的丸激素,CFAP61 knockdown使男性不孕症恶化

Wenkai Zhu¹, Jing Mao¹, Jianxin Qin¹

¹Department of Histology and Embryology, Medical School of Nantong University, No. 19, Qixiu Road, Chongchuan District, Nantong, 226001, Jiangsu, China.

Functional & integrative genomics

|November 20, 2023

概括

纤毛和鞭毛相关蛋白61 (CFAP61) 对于男性生育能力至关重要. 低水平的CFAP61会损害莱迪格细胞的功能并增加细胞亡,这表明CFAP61是男性不孕症的治疗点.

科学领域:

生殖生物学生殖生物学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

男性不孕症影响了生殖年龄人口的很大一部分.
乳毛和鞭毛相关的蛋白质在精子功能和男性生殖健康中起着至关重要的作用.
CFAP61在男性不孕症中的特定作用在很大程度上仍未被探索.

研究的目的:

研究CFAP61在男性不孕症中的表达和功能.
阐明CFAP61影响莱迪格细胞功能和男性生育能力的潜在分子机制.
评估CFAP61作为男性不孕症治疗点的潜力.

主要方法:

定量实时聚合酶连锁反应 (qRT-PCR) 和西部涂抹来评估CFAP61表达.
免疫组织化学测定用于在丸组织中定位CFAP61.
细胞计数套件-8,5-乙烯基-2'-脱氧氨酸 (EdU) 结合,流细胞计和酶相关的免疫吸收试验 (ELISA) 以评估莱迪格细胞活力,增殖,亡和分泌.

主要成果:

在不育男性的丸组织中,CFAP61的表达显著降低.
CFAP61敲击降低了莱迪格细胞活力和丸激素分泌,同时增加了亡.
沉默CFAP61激活了基激活蛋白激酶 (MAPK) /环氧激酶-2 (COX-2) 信号通路,通过增加p-ERK,p-JNK,p-P38和COX-2水平来证明这一点.

结论:

CFAP61在维持莱迪格细胞功能和男性生育能力方面发挥着至关重要的作用.
降低CFAP61的调节有助于男性不育,通过损害莱迪格细胞活力,激素的产生,并通过MAPK/COX-2通路促进细胞亡.
CFAP61代表了治疗男性不孕症的潜在治疗标.

关键词:

在CFAAP61中使用.莱迪格细胞是莱迪格细胞.通过MAPK/COX-2通路进行.男人不孕不育的情况丸激素分泌的分泌物

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