Involvement of autophagy in germ cells in an experimental model of varicocele in rats before and after varicocelectomy
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Read the article on link.springer.com ↗Article · Dec 2024 · 1 min read
In brief
In brief
This rat model study demonstrates that varicocele activates autophagy markers in testicular germ cells, contributing to impaired spermatogenesis. While surgical varicocelectomy improves histological scores, autophagy markers remain elevated post-surgery, suggesting persistent cellular dysfunction despite treatment.
- Varicocele significantly activates autophagy markers (LC3A, Beclin-1, Ambra-1, ULK-1, p62) in testicular germ cells compared to controls.
- Surgical varicocelectomy improves spermatogenesis scores but does not fully normalize autophagy marker expression.
- Persistent autophagy activation post-surgery suggests ongoing germ cell dysfunction despite histological improvement.
- p62 expression paradoxically increases in varicocele, indicating potential modulatory role beyond its known autophagy inhibition.
- Early surgical intervention may be warranted given incomplete reversal of cellular stress pathways after varicocelectomy.
Written by the GCMD Library team from the article.
Abstract
Introduction
Autophagy, a catabolic process enabling cellular organelles and proteins’ reuse for energy, has been observed in varicocele models, but the effect of surgical treatment on this process remains unknown. This study aims to assess autophagy in varicocele models undergoing surgical correction.
Materials and Methods
Twenty-one adolescent male rats were induced with varicocele and divided into three groups: sham, varicocele, and varicocele with varicocelectomy. After 21 days, testicles were examined histologically for spermatogenesis (Jonhsen’s score) and immunohistochemically for autophagy markers (LC3A, Beclin-1, Ambra-1, ULK-1, p62). Positive germ cells were quantitatively evaluated, and data were statistically analyzed (p < 0.05).
Results
Histological examination revealed significantly reduced Jonhsen’s scores in varicocele compared to sham and varicocelectomy groups (p < 0.05). Expression of autophagy markers (LC3A, Beclin-1, Ambra-1, ULK-1, p62) was significantly higher in varicocele than sham and varicocelectomy groups (p < 0.05), and in varicocelectomy than sham (p < 0.05).
Conclusions
Varicocele activates autophagy markers, with p62 potentially modulating autophagy despite being considered an inhibitor. While varicocelectomy improves histology, it doesn’t fully inhibit autophagy, suggesting ongoing germ cell dysfunction despite treatment. This underscores varicocele’s detrimental effects on germ cell functionality.
