期刊
CELLS
卷 8, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/cells8060629
关键词
aging; sperm quality; signaling proteins; mTORC1; TP53
类别
资金
- FEDER funds through the Programa Operacional Competitividade e Internacionalizacao COMPETE 2020
- FCT Fundacao para a Ciencia e Tecnologia [PTDB/BBB-BQB/3804/2014]
- iBiMED [UID/BIM/04501/2013, POCI-01-0145-FEDER-007628]
- Integrated Program of SR&TD pAGE-Protein aggregation Across the Lifespan
- Centro 2020 program, Portugal 2020, European Union, through the European Regional Development Fund [CENTRO-01-0145-FEDER-000003]
- FCT [SFRH/BPD/123155/2016]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/123155/2016] Funding Source: FCT
Understanding how age affects fertility becomes increasingly relevant as couples delay childbearing toward later stages of their lives. While the influence of maternal age on fertility is well established, the impact of paternal age is poorly characterized. Thus, this study aimed to understand the molecular mechanisms responsible for age-dependent decline in spermatozoa quality. To attain it, we evaluated the impact of male age on the activity of signaling proteins in two distinct spermatozoa populations: total spermatozoa fraction and highly motile/viable fraction. In older men, we observed an inhibition of the mechanistic target of rapamycin complex 1 (mTORC1) in the highly viable spermatozoa population. On the contrary, when considering the entire spermatozoa population (including defective/immotile/apoptotic cells) our findings support an active mTORC1 signaling pathway in older men. Additionally, total spermatozoa fractions of older men presented increased levels of apoptotic/stress markers [e.g., cellular tumor antigen p53 (TP53)] and mitogen-activated protein kinases (MAPKs) activity. Moreover, we established that the levels of most signaling proteins analyzed were consistently and significantly altered in men older than 27 years of age. This study was the first to associate the mTOR signaling pathway with the age impact on spermatozoa quality. Additionally, we constructed a network of the sperm proteins associated with male aging, identifying TP53 as a central player in spermatozoa aging.
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