Impacts of varicocele on the structure and proteomics of rat testis tissue: An experimental study.
- Author:
Xu-Song ZHAO
1
;
Bo FANG
1
;
Cang-Yu TIAN
1
;
Yan-Kang CUI
1
;
Tian-Yi SHEN
1
;
Su-Chun WANG
1
;
Hao TANG
2
;
Meng WU
3
;
Feng XU
1
Author Information
1. Department of Urology, Jinling Hospital Affiliated to Nanjing University School of Medicine / General Hospital of Eastern Theater Command, Nanjing, Jiangsu 210002, China.
2. .
3. Wujin Hospital of TCM/Affiliated Hospital of Nanjing University of Chinese Medicine， Jiangsu 213161, China.
- Publication Type:Journal Article
- Keywords:
varicocele;
high ligation of spermatic vein;
testis tissue;
differential proteins;
rat
- MeSH:
Male;
Animals;
Varicocele/pathology*;
Rats;
Testis/ultrastructure*;
Rats, Sprague-Dawley;
Proteomics;
Signal Transduction;
Proteome
- From:
National Journal of Andrology
2024;30(12):1098-1104
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the impacts of varicocele (VC) and varicocelectomy (VCT) on the proteomics of rat testis tissue, and to analyze the differential proteins and signaling pathways, and observe the microstructural changes of the testis tissue.
METHODS:We selected 60 male SD rats and divided them into a sham operation (SO), a VC model control, and a VCT group. We harvested the testis tissues from the rats at 4 weeks after modeling for determination of the differential protein expressions by mass spectrometry, analysis of the changes in the protein signaling pathways by KEGG pathway repolarization, and observation of the microstructural changes in the spermatogenic cells under the transmission electron microscope (TEM).
RESULTS:A total of 15 clinically significant proteins were effectively identified, among which RPS24, KIFAP3, HPX, RPL38, TOP2A, PRPF19, TRPM3, RPL32, CNBP and AHSG were upregulated, while RPS9, TKFC, SH3BGRL3, ACAA2 and FABP3 downregulated. The differential pathways found included the Type-I 4-aminobutyrate degradation pathway, eIF2 signaling pathway, and Type-III glutamate degradation pathway, which were all related to the pathogenesis of testicular growth arrest. Compared with the rats in the VCT group, those of the VC group rats showed ultrastructural changes in the testis tissue under the TEM, such as mitochondrial vacuolar degeneration, dense nucleoli, invagination of cell nuclear membranes, and irregularity, which were detrimental to the survival of testicular cells.
CONCLUSION:VCT affects the development and growth of the testis by altering the expressions of relevant proteins and influencing the changes of the gene pathways in the testicular cells, which may be one of the causes of VC inducing testis injury and testicular spermatogenic dysfunction. The changes in these molecular pathways can provide some theoretical evidence for an insight VC as well as potential therapeutic targets for its treatment.
