Deletion of Sox30 in mice uniquely impairs testis development and spermatogenesis with complete absence of spermatozoa in testes leading to male infertility, but does not influence ovary development and female fertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
The purpose of the study was to investigate whether the promoter methylation status of BRCA1 and BRCA2 DNA repair genes is associated with sperm DNA fragmentation (sDF) in infertile men with oligoasthenoteratozoospermia (OAT) which emerges due to various reasons and is effective in male infertility.
In conclusion, capacity of seminal plasma for producing DNA cleavage represents a solid contribution to expand the analysis of the standard seminal profile and could constitute a putative diagnostic tool for evaluating male infertility.<b>Abbreviations:</b> ALS: alkali labile sites; ART: Assisted Reproduction Technologies; DBD-FISH: DNA Breakage Detection-Fluorescence In Situ Hybridization; DNA: deoxyribonucleic acid; DSBs-DNA: double-strand DNA; FITC: Fluorescein IsoThioCyanate; GEDA: Gravity Enforced Diffusion Assays; PBS: phosphate-buffered saline; ROS: Reactive Oxigen Species; SSBs-DNA: single-strand DNA; SSC: saline-sodium citrate.
In contrast to the meiotic role of Sycp3, CRISPR-loxP-mediated multi-megabase deletions of the Slx (5 Mb) and Slxl1 (2.3Mb) ampliconic regions result in post-meiotic defects, abnormal sperm, and male infertility.
Collectively, these results implicate that miR-509-5p may participate in the pathogenesis of male infertility and TGCT through regulating proliferation and apoptosis, two critical cellular activities for spermatogenesis and TGCT tumorigenesis.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
The study indicated that miR-125b-2 had a positive influence on the reproductive performance of animals by regulating the expression of the PAP gene, and could be a potential drugs and diagnostic target for male infertility.
To evaluate the contribution of copy number variations of E2F1 gene to idiopathic male infertility and the factors influencing expression of this gene.
PIWI-LIKE 1 and PIWI-LIKE 2 mRNA expression exhibited a significant association with impaired sperm characteristics and may be a useful candidate for the evaluation of the impact of PIWI-LIKE 1-4 mRNA expression on male infertility.
Therefore, these results demonstrate that inhibition of p38 activity prevents CdCl<sub>2</sub>-induced apoptotic GC-2spd cell death by reducing depolarization of mitochondrial membrane potential and mitochondrial ROS levels via ERK phosphorylation in a signal pathway different from the CdCl<sub>2</sub>-induced ERK/Drp1/p38 axis and suggest a therapeutic strategy for CdCl<sub>2</sub>-induced male infertility.
The study indicated that miR-125b-2 had a positive influence on the reproductive performance of animals by regulating the expression of the PAP gene, and could be a potential drugs and diagnostic target for male infertility.
In this review, we discuss the association of PCD genes and other axonemal genes with male infertility, drawing particular attention to possible differences between their functions in motile cilia and sperm tails.
Depletion of the major outer dense fiber protein 1 (ODF1) mainly caused decapitation and male infertility but validated binding partners collaborating in the formation of sperm-specific structures are largely unknown.
Our results uncover a previously unknown physiological role of NCOA5 in the regulation of epididymal sperm maturation and suggest that NCOA5 deficiency could cause male infertility through increased IL-6 expression in epididymis.
Pdzk1 protein level was also reduced in the spermatozoa in case of asthenozoospermic patients compared with that in normozoospermic men, suggesting that Pdzk1 may participate in sperm maturation regulation and may be associated with male infertility.
The pairs hsa-miR-942-5p/hsa-miR-1208 and hsa-miR-34b-3p/hsa-miR-93-3p have the potential to become new molecular biomarkers that could help to diagnose male infertility, especially in cases of UMI or when seminal parameters are close to the threshold values.