ArticleTranslational andrology and urology2024
External pressure induces the dysfunction of spermatogonia via triggering the intrinsic pathway of apoptosis.
Article in Translational andrology and urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Cryptorchidism and infertility: what do we know so far?Asian journal of andrology · 2026Review
- The Molecular Mechanism of a Complex1-induced Apoptosis in Cancer Cells of the Esophagus.Current molecular medicine · 2026Article
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8 authors.
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Abstract
Background: Cryptorchidism, the failure of testes to descend into the scrotum, exposes the testes to higher temperature and external pressure. Scholars from Razi University found through research conducted at different pressure gradients (0, 25, 50, and 100 mmHg) and time gradients (2 and 4 h) that high hydrostatic pressure may lead to sperm apoptosis. In this work, we investigated the effect of external pressure on spermatogonia, exploring a new mechanism of male infertility caused by cryptorchidism. Methods: Various pressure gradients (0, 25, 50, and 100 mmHg) were applied to spermatogonia for different durations (0, 2, and 4 h) in the Cell Counting Kit-8 (CCK8) experiment. Morphological changes, cell ultrastructure, apoptosis rates, and the expression of apoptosis-related proteins (bax, bcl-2, caspase-3, and caspase-9) were assessed through immunofluorescence, electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay, flow cytometry, immunohistochemistry, real-time quantitative polymerase chain reaction (qPCR), and western blot. Results: The cell viability assay showed that higher external pressure had a greater negative time-dependent impact on cell viability. Immunofluorescence results indicated that external pressure stimuli altered the morphology of spermatogonia. The results of TUNEL assay and flow cytometry demonstrated that external pressure stimuli induced apoptosis in spermatogonia. Transmission electron microscopy (TEM) observations showed the generation of apoptotic bodies, mitochondrial swelling, vacuolization, and mitochondrial cristae fusion. The results of immunohistochemistry indicated that pressure induced the expression of caspase-3 and caspase-9 proteins. qPCR and western blot analyses revealed an increased ratio of bax/bcl-2 and expression of caspase-3 and caspase-9. Methazolamide (cytochrome C inhibitor) blocked the pressure-induced cell apoptosis and inhibited the activation of caspase-3 while Z-IETD-FMK (caspase-8 inhibitor) did not. Conclusions: External pressure promotes spermatogonia apoptosis through the intrinsic apoptosis pathway, which may be one of the mechanisms of male infertility induced by cryptorchidism.
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