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3
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4
Chronic exposures and male fertility: the impacts of environment, diet, and drug use on spermatogenesis.慢性暴露与男性生育能力:环境、饮食及药物使用对精子发生的影响。
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9
Spermatogenesis, DNA damage and DNA repair mechanisms in male infertility.男性不育中的精子发生、DNA损伤与DNA修复机制
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在生精功能障碍患者的睾丸中,MRE11 和 RAD50 的表达降低。

Decreased expression of MRE11 and RAD50 in testes from humans with spermatogenic failure.

机构信息

Department of Reproductive Endocrinology, Women's Hospital, Zhejiang University School of Medicine, 1 Xueshi Road, Hangzhou, 310006, Zhejiang, China.

Department of Gynecology, Weifang Maternal and Child Health Hospital, Weifang, 261000, China.

出版信息

J Assist Reprod Genet. 2020 Feb;37(2):331-340. doi: 10.1007/s10815-019-01686-5. Epub 2020 Jan 25.

DOI:10.1007/s10815-019-01686-5
PMID:31983050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7056783/
Abstract

PURPOSE

To assess testicular mRNA and protein expression levels of MRE11 and RAD50 in human azoospermia patients.

METHODS

Patients diagnosed with maturation arrest at the spermatocyte stage (MA) and Sertoli cell-only syndrome (SCOS) were recruited through diagnostic testicular biopsy. Patients with normal spermatogenesis were studied as controls. In addition, knockdown of MRE11 and RAD50 was performed in GC-2spd(ts) cells to investigate their roles in cellular proliferation and apoptosis.

RESULTS

mRNA and protein expression levels of MRE11 and RAD50 were measured using quantitative polymerase chain reaction, western blotting, and immunohistochemistry, respectively. Knockdown of both MRE11 and RAD50 utilized transfection with small interfering RNAs.

CONCLUSION

Our findings demonstrated altered expression levels of MRE11 and RAD50 in human testes with MA and SCOS, and showed that these alterations might be associated with impaired spermatogenesis. These results offer valuable new perspectives into the molecular mechanisms of male infertility.

摘要

目的

评估人类非梗阻性无精子症患者睾丸中 MRE11 和 RAD50 的 mRNA 和蛋白表达水平。

方法

通过诊断性睾丸活检招募被诊断为精母细胞阶段阻滞(MA)和唯支持细胞综合征(SCOS)的患者作为研究对象。正常精子发生的患者作为对照组进行研究。此外,在 GC-2spd(ts)细胞中敲低 MRE11 和 RAD50,以研究它们在细胞增殖和凋亡中的作用。

结果

使用定量聚合酶链反应、蛋白质印迹和免疫组织化学分别测量 MRE11 和 RAD50 的 mRNA 和蛋白表达水平。使用小干扰 RNA 转染进行 MRE11 和 RAD50 的敲低。

结论

我们的研究结果表明,MA 和 SCOS 患者睾丸中 MRE11 和 RAD50 的表达水平发生改变,并且这些改变可能与受损的精子发生有关。这些结果为男性不育的分子机制提供了有价值的新视角。