About Us |
PMID | 29581387 |
Gene Name | RNASET2 |
Condition | Reduced sperm motility |
Association |
Associated |
Population size | 205 |
Population details | 205 semen samples from both asthenozoospermia patients, normozoospermia individuals |
Sex | Male |
Infertility type | Male infertility |
Other associated phenotypes |
Reduced sperm motility |
RNASET2 impairs the sperm motility via PKA/PI3K/calcium signal pathways Xu Y, Fan Y, Fan W, Jing J, Xue K, Zhang X, Ye B, Ji Y, Liu Y, Ding Z. Asthenozoospermia is one of the leading causes of male infertility owing to a decline in sperm motility. Herein, we determined if there is a correlation between RNASET2 content on human spermatozoa and sperm motility in 205 semen samples from both asthenozoospermia patients and normozoospermia individuals. RNASET2 content was higher in sperm from asthenozoospermia patients than in normozoospermia individuals. On the other hand, its content was inversely correlated with sperm motility as well as progressive motility. Moreover, the inhibitory effect of RNASET2 on sperm motility was induced by incubating normozoospermic sperm with RNase T2 protein. Such treatment caused significant declines in intracellular spermatozoa PKA activity, PI3K activity and calcium level, which resulted in severely impaired sperm motility, and the sperm motility was largely rescued by cAMP supplementation. Finally, protein immunoprecipitation and mass spectrometry identified proteins whose interactions with RNASET2 were associated with declines in human spermatozoa motility. AKAP4, a protein regulating PKA activity, coimmunoprecipated with RNASET2 and they colocalized with one another in the sperm tail, which might contribute to reduced sperm motility. Thus, RNASET2 may be a novel biomarker of asthenozoospermia. Increases in RNASET2 can interact with AKAP4 in human sperm tail and subsequently reduce sperm motility by suppressing PKA/PI3K/calcium signaling pathways. CI - © 2018 Society for Reproduction and Fertility. FAU - Xu, Yali AU - Xu Y AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Fan, Yong AU - Fan Y AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. AD - Department of Assisted ReproductionShanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Fan, Weimin AU - Fan W AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. AD - Reproductive Medicine CenterShanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Jing, Jia AU - Jing J AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Xue, Ke AU - Xue K AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Zhang, Xing AU - Zhang X AD - Department of Clinical MedicineSchool of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Ye, Bin AU - Ye B AD - Department of Clinical MedicineSchool of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Ji, Yingjie AU - Ji Y AD - Department of Clinical MedicineSchool of Medicine, Shanghai Jiao Tong University, Shanghai, China. FAU - Liu, Yue AU - Liu Y AD - Department of HistologyEmbryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, School of Medicine, Shanghai Jiao Tong University, Shanghai, China liuyue@shsmu.edu.cn zding@shsmu.edu.cn. |