Seco-Rovira Vicente, Martínez-Hernández Jesús, Freire-Brito Laís, Beltrán-Frutos Ester, Madrid Juan Francisco, Pastor Luis Miguel
Department of Cell Biology and Histology, Medical School, Biomedical Research Institute of Murcia Pascual Parrilla-IMIB, Regional Campus of International Excellence "Campus Mare Nostrum", University of Murcia, 30120 Murcia, Spain.
Clinical and Experimental Endocrinology, UMIB-Unit for Multidisciplinary Research in Biomedicine, ICBAS-School of Medicine and Biomedical Science, University of Porto, 4050-313 Porto, Portugal.
Animals (Basel). 2025 Jun 8;15(12):1696. doi: 10.3390/ani15121696.
In testicular pathology, the accumulation of extracellular matrix and thickening of the peritubular lamina propria are associated with altered spermatogenesis. This study evaluated the immunoexpression of certain proteins in Sertoli and myoid cells of cryptorchid boar seminiferous tubule sections to determine the role of these cells in peritubular lamina propria thickening. Sections of normal seminiferous tubules and those with varying degrees of atrophy (I-III) were studied using histochemical and immunohistochemical techniques. A semiquantitative analysis of histochemical staining or immunostaining intensity in these sections was performed. Gradual thickening of the peritubular lamina propria was observed between stage II and III sections. HSP47 was present in myoid and Sertoli cells in normal sections and was significantly increased in stage II and III sections. The increase in stage II was dependent on Sertoli cells, while in stage III, it depended on myoid cells. The vimentin increases in stage I sections were due to Sertoli cells and later to myoid cells in stages II and III. α-actin and collagen IV immunoreactivity were observed from the early stage of atrophy, with a significant increase in stage III. In conclusion, in porcine spontaneous cryptorchidism, the seminiferous tubule exhibits gradual fibrotic alterations in the peritubular lamina propria, initially related to changes in the Sertoli cell phenotype and later, in the final stages, to myoid cells. Collagen I deposition appears to be caused by myoid cells, initiating the sclerosis of the seminiferous tubules.
在睾丸病理学中，细胞外基质的积累和生精小管固有层的增厚与精子发生改变有关。本研究评估了隐睾公猪生精小管切片中支持细胞和肌样细胞中某些蛋白质的免疫表达，以确定这些细胞在生精小管固有层增厚中的作用。使用组织化学和免疫组织化学技术研究了正常生精小管切片以及具有不同程度萎缩（I - III级）的切片。对这些切片中的组织化学染色或免疫染色强度进行了半定量分析。在II期和III期切片之间观察到生精小管固有层逐渐增厚。HSP47在正常切片的肌样细胞和支持细胞中存在，在II期和III期切片中显著增加。II期的增加依赖于支持细胞，而在III期，则依赖于肌样细胞。波形蛋白在I期切片中的增加归因于支持细胞，在II期和III期则归因于肌样细胞。α - 肌动蛋白和IV型胶原免疫反应性从萎缩早期就可观察到，在III期显著增加。总之，在猪自发性隐睾症中，生精小管在生精小管固有层呈现逐渐的纤维化改变，最初与支持细胞表型变化有关，在后期，即最后阶段，与肌样细胞有关。I型胶原沉积似乎由肌样细胞引起，启动了生精小管的硬化。
