Nicotine elevates sperm motility and induces Pfn1 promoter hypomethylation in mouse testis

被引：24

作者：

Dai, J. ^{[1
]}

Zhan, C. ^{[1
]}

Xu, W. ^{[1
]}

Wang, Z. ^{[1
]}

Nie, D. ^{[1
]}

Zhao, X. ^{[1
]}

Zhang, D. ^{[1
]}

Gu, Y. ^{[1
]}

Wang, L. ^{[1
]}

Chen, Z. ^{[2
]}

Qiao, Z. ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Life Sci & Biotechnol, Shanghai Peoples Hosp 6, Shanghai 200240, Peoples R China

[2] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 6, Dept Urol, Shanghai 200240, Peoples R China

来源：

ANDROLOGY | 2015年 / 3卷 / 05期

关键词：

cytoskeleton; nicotine; profilin; proteomics; sperm motility; testis; CIGARETTE-SMOKING; IN-VITRO; ACTIN; EXPOSURE; METHYLATION; EXPRESSION; COTININE;

D O I：

10.1111/andr.12072

中图分类号：

R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

摘要：

Many studies have addressed the hazardous role of cigarette smoking on male fertility, but the exact molecular mechanisms involved in the impairments caused by nicotine remain unclear. To evaluate the detrimental effects of nicotine exposure on spermatogenesis, two-dimensional gel electrophoresis and mass spectrometry analysis were performed to screen and identify differentially expressed proteins from the testes of mice exposed to nicotine daily. Data mining analysis indicated that the 15 identified proteins were mainly involved in actin cytoskeleton regulation and in the tricarboxylic acid cycle, which are related to cell motility. Further investigation of a central regulatory factor in the cytoskeleton regulation, profilin 1 (PFN1), revealed that nicotine-induced Pfn1 over-expression in mouse testes, specifically in elongated spermatids, by Pfn1 promoter hypomethylation. Interestingly, elevated sperm motility parameters were observed in nicotine-treated mice. We assume that nicotine-induced PFN1 over-expression in mouse spermatids may promote actin polymerization and ultimately enhance sperm motility.

引用

页码：967 / 978

页数：12

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