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Published on: February 6, 2018
Syncytin-a deficiency compromises murine sperm function by suppressing PRL/PGE2 and PI3K/AKT/mTOR pathway
Qianqian Wang1,2,3, Zhenwei Wang4, Zhenpeng Li4
1Department of Pathophysiology, Shandong Second Medical University, Weifang, Shandong 261053, P.R. China.
Abstract:
The human endogenous retrovirus W envelope protein syncytin-1 (syncytin-a in mus) can be involved in fetal development and tumorigenesis. The role of syncytin-1 in male infertility has not been identified. In this study, the prostatic epithelial-specific syncytin-a knockout (syna CKO) mouse model was constructed. First, male infertility, abnormal testicular seminiferous tubule, and prostate gland were discovered in syna CKO mice. Then, irregular sperm motility, morphology, and MMAF-associated gene expression (AKAP3, SPAG6) were detected in syna CKO mice. Increased prostaglandin E2 (PGE2) and prolactin (PRL) modulate the lipid metabolism of the testis in syna CKO mice. Syna CKO with inhibitor or activator treatment identified that syna knockout could inhibit the PI3K/AKT/mTOR pathway, Ca2+ levels, and elevate caspase 3 expression. Therefore, we propose a hypothesis that syna deficiency exacerbates testicular lipid accumulation and apoptosis by suppressing the PI3K/AKT/mTOR and Ca2+ pathway, ultimately leading to spermatogenic dysfunction and male infertility.
Insights
Syncytin-1 deficiency in mice causes male infertility by disrupting sperm health and testicular function. This involves altered lipid metabolism and apoptosis, highlighting syncytin-1
Area of Science:
- Reproductive biology
- Endocrinology
- Genetics
Background:
- Human endogenous retrovirus W envelope protein syncytin-1 (syncytin-a in mice) is implicated in development and cancer.
- Its role in male infertility remains uncharacterized.
Purpose of the Study:
- To investigate the function of syncytin-a in male reproductive health.
- To elucidate the molecular mechanisms underlying syncytin-a deficiency-induced male infertility.
Main Methods:
- Construction of a prostatic epithelial-specific syncytin-a knockout (syna CKO) mouse model.
- Analysis of male reproductive parameters, sperm characteristics, and gene expression.
- Investigation of signaling pathways (PI3K/AKT/mTOR, Ca2+) and apoptosis markers.
Main Results:
- Syna CKO mice exhibited male infertility, abnormal testicular and prostate structures.
- Sperm motility, morphology, and MMAF-associated gene expression (AKAP3, SPAG6) were irregular.
- Increased prostaglandin E2 (PGE2) and prolactin (PRL) affected testicular lipid metabolism.
- Syncytin-a knockout inhibited the PI3K/AKT/mTOR pathway and Ca2+ levels, while elevating caspase 3 expression.
Conclusions:
- Syncytin-a deficiency exacerbates testicular lipid accumulation and apoptosis.
- Suppression of PI3K/AKT/mTOR and Ca2+ pathways contributes to spermatogenic dysfunction.
- Syncytin-a plays a crucial role in maintaining male fertility.
