Objective: To examine the effect of Ureaplasma parvum (U. parvum) infection on mouse sperm motility, structure, and fertilizing ability and on embryo development.
Design: In vitro model of the effects of U. parvum serovar 3 infection on mouse sperm.
Setting: Basic research laboratory.
Intervention(s): None.
Animals: Mice.
Main Outcome Measure(s): Mouse sperm motility was examined using the swim-up method, and their motility parameters were analyzed using the sperm motility analysis system. Localization and invasion of U. parvum were observed with fluorescence, confocal, and scanning electron microscopy. After in vitro fertilization with U. parvum-infected sperm, the quality of the fertilized egg and embryo development were assessed.
Result(s): U. parvum was attached and internalized into mouse sperms and localized mainly at the sperm head and midpiece. U. parvum-infected mouse sperms exhibited decreased motility in a dose- and duration-dependent manner. Electron micrographs revealed that U. parvum infection induced the aggregation and morphological destruction of mouse sperm. Infected mouse sperm transported U. parvum into the fertilized egg with reduced fertilization rates, and infected embryo development was impaired.
Conclusion(s): U. parvum infection caused deterioration of the mouse sperm quality and its functions, which affected the fertilization rate and embryo development.
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http://dx.doi.org/10.1016/j.xfss.2020.12.003 | DOI Listing |
Commun Biol
January 2025
Université Paris Cité, CNRS, Inserm, Institut Cochin, F-75014, Paris, France.
The H3K79 methyltransferase DOT1L is essential for multiple aspects of mammalian development where it has been shown to regulate gene expression. Here, by producing and integrating epigenomic and spike-in RNA-seq data, we decipher the molecular role of DOT1L during mouse spermatogenesis and show that it has opposite effects on gene expression depending on chromatin environment. On one hand, DOT1L represses autosomal genes that are devoid of H3K79me2 at their bodies and located in H3K27me3-rich/H3K27ac-poor environments.
View Article and Find Full Text PDFMol Reprod Dev
January 2025
Department of Anatomy, Histology, Forensic Medicine and Orthopedic, Section of Histology, Sapienza University of Rome, Rome, Italy.
A role for the plasminogen activator (PA) system has been postulated in mammalian gonads, considering the complex process of morphogenesis these organs undergo during their development. Our results show that mouse Sertoli cells under basal conditions produce both types of PA, tissue-type PA (tPA) and urokinase-type PA (uPA), and hormonal treatments increase the production of both enzymes. The increased enzyme secretion does not correlate with a parallel increase in their mRNAs.
View Article and Find Full Text PDFACS Nano
January 2025
Department of Urology, Peking University First Hospital, Beijing 100034, China.
Although considered an "eco-friendly" biodegradable plastic, polylactic acid (PLA) microplastic (PLA-MP) poses a growing concern for human health, yet its effects on male reproductive function remain underexplored. This study investigated the reproductive toxicity of PLA in male mice and its potential mechanisms. To this end, our in vivo and in vitro experiments demonstrated that after degradation in the digestive system, a significant number of PLA-MP-derived nanoparticles could penetrate the blood-testis barrier (BTB) and localize within the spermatogenic microenvironment.
View Article and Find Full Text PDFNucleic Acids Res
January 2025
Institute of Reproductive Medicine, School of Medicine, Nantong University, Nantong 226001, China.
Chromatin remodeling, which involves the histone-to-protamine exchange process during spermiogenesis, is crucial for sperm nuclear condensation and male fertility. However, the key regulators and underlying molecular mechanisms involved in this process remain largely unexplored. In this study, we discovered that deficiency in the family with sequence similarity 170 member A (Fam170a) led to abnormal sperm nuclear morphology and male infertility in mice, mirroring the observation of very low Fam170a transcription levels in sperm of infertile men with teratozoospermia.
View Article and Find Full Text PDFEpigenetics
December 2025
Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA, USA.
The effects of chronically stressing male mice can be transmitted across generations by stress-specific changes in their sperm miRNA content, which induce stress-specific phenotypes in their offspring. However, how each stress paradigm alters the levels of distinct sets of sperm miRNAs is not known. We showed previously that exposure of male mice to chronic social instability (CSI) stress results in elevated anxiety and reduced sociability specifically in their female offspring across multiple generations because it reduces miR-34c levels in sperm of stressed males and their unstressed male offspring.
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