Male juvenile spermatogonial depletion (jsd/jsd) mice are sterile because of a failure of spermatogonial differentiation. We have previously reported the recovery of spermatogonial differentiation by suppressing the levels of gonadotropins and testosterone with Nal-Glu, a GnRH antagonist. To determine whether suppression of testosterone or the gonadotropins was responsible for spermatogenic recovery, we examined the effect of supplementation of LH or FSH along with Nal-Glu treatment. Systemic administration of flutamide, an androgen receptor antagonist, was also examined. LH supplementation elevated both serum and intratesticular testosterone levels and suppressed the recovery of spermatogonial differentiation in a dose-dependent manner. Supplementation with FSH did not affect either testosterone levels or spermatogonial differentiation. Furthermore, the mice treated with flutamide showed some recovery of spermatogonial differentiation. The overall findings revealed that testosterone action mediated by androgen receptors suppressed the spermatogonial differentiation in jsd/jsd mice and suggested that spermatogonial differentiation in the jsd mutant is highly sensitive to testosterone suppression.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1095/biolreprod65.2.532 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cdkn1c orchestrates a molecular network that regulates the euploidy of the male mouse germline stem cells.
Development
January 2025
Department of Molecular Genetics, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Karyotype instability in the germline leads to infertility. Unlike the female germline, the male germline continuously produces fertile sperm throughout life. Here we present a molecular network responsible for maintaining karyotype stability in the male mouse germline.
View Article and Find Full Text PDFSystematic identification of Y-chromosome gene functions in mouse spermatogenesis.
Science
January 2025
Sex Chromosome Biology Laboratory, The Francis Crick Institute, London, UK.
The mammalian Y chromosome is essential for male fertility, but which Y genes regulate spermatogenesis is unresolved. We addressed this by generating 13 Y-deletant mouse models. In , , and deletants, spermatogenesis was impaired.
View Article and Find Full Text PDFTranscriptomic dynamics and cell-to-cell communication during the transition of prospermatogonia to spermatogonia revealed at single-cell resolution.
BMC Genomics
January 2025
Key Laboratory of Adaptation and Evolution of Plateau Biota, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai, 810008, China.
Background: Spermatogonia are essential for the continual production of sperm and regeneration of the entire spermatogenic lineage after injury. In mammals, spermatogonia are formed in the neonatal testis from prospermatogonia (also termed gonocytes), which are established from primordial germ cells during fetal development. Currently, the molecular regulation of the prospermatogonial to spermatogonia transition is not fully understood.
View Article and Find Full Text PDFFrom spermatogenesis to fertilisation: the role of melatonin on ram spermatozoa.
Domest Anim Endocrinol
January 2025
BIOFITER-IUCA, Universidad de Zaragoza, Facultad de Veterinaria, Miguel Servet 177, 50013 Zaragoza, Spain. Electronic address:
This review presents recent findings on the effect of melatonin on ram spermatozoa. This hormone regulates seasonal reproduction in the ovine species through the hypothalamic-pituitary-gonadal axis, but it also exerts direct effects on spermatogenesis, seminal quality and fertility. In the testis, melatonin stimulates blood flow to this organ, but it also appears to be involved in the differentiation of spermatogonial stem cells and the secretion of testosterone through the MT1 and MT2 receptors.
View Article and Find Full Text PDFProgress in the Study of TAp73 and Sperm Apoptosis.
Cell Biochem Funct
January 2025
Department of Physiology and Pharmacology, Anhui University of Chinese Medicine, Hefei, Anhui, China.
The study of the mechanism of oligoasthenospermia, which is a major cause of male infertility, has been the focus of research in the field of male reproduction. TAp73, a member of the p53 family of oncogenes, is endowed with tumor-suppressing activity due to its structural and functional homology with p53. It has been found that TAp73, plays a key role in spermatogenesis and maintaining male reproduction.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!