Gao Yuanyuan, Xu Shumin, Qiao Jiajun, Wang Chen, Wang Kaixian, Sun Junpei, Liu Lei, Li Leina, Liang Meng, Hu Ke
School of Life Science, Bengbu Medical University, Bengbu, Anhui, People's Republic of China.
First Affiliated Hospital, Bengbu Medical University, Bengbu, Anhui, People's Republic of China.
Cells Dev. 2024 Sep;179:203925. doi: 10.1016/j.cdev.2024.203925. Epub 2024 May 24.
Undescended testis (UDT), known as cryptorchidism (CRY), is a common congenital disorder in which one or both testicles do not descend normally into the scrotum. A unilateral UDT model was established by inducing UDT in mice through surgery. The results showed that the testis in the UDT model group was abnormal; the lumen of the seminiferous tubule was atrophic; apoptosis, necrosis and shedding were observed in many of the germ cells; the level of sex hormones was abnormal; and mature sperm was reduced. Subsequently, transcriptome sequencing was conducted on the testicular tissue of UDT model mice. Through analysis and verification of differential genes, AZIN2 was identified as playing a key role in the decline in male fertility caused by cryptorchidism. AZIN2 expression and spermine content was down-regulated in the testis of the UDT group. We then used a combination of hypoxanthine and xanthine to create a GC-1 cell damage model. In this model, AZIN2 expression and spermine content was down-regulated. When si-Azin2 transfected GC-1 cells, cell viability and proliferation were decreased. However, in the GC-1 cell damage model transfected with Azin2 over-expressed plasmid, AZIN2 expression and spermine content was up-regulated, reversing the cell damage caused by hypoxanthine and xanthine, and restoring the proliferation ability of GC-1 cells. These results indicate that in UDT, down-regulated AZIN2 expression is a factor in testicular damage. This discussion of the connection between AZIN2 and germ cells has important clinical significance as it provides an important reference for the diagnosis and treatment of cryptorchidism.
隐睾（UDT），又称睾丸未降（CRY），是一种常见的先天性疾病，其中一个或两个睾丸不能正常降入阴囊。通过手术诱导小鼠发生隐睾来建立单侧隐睾模型。结果显示，隐睾模型组的睾丸异常；生精小管管腔萎缩；许多生殖细胞出现凋亡、坏死和脱落；性激素水平异常；成熟精子减少。随后，对隐睾模型小鼠的睾丸组织进行转录组测序。通过对差异基因的分析和验证，确定AZIN2在隐睾导致的男性生育力下降中起关键作用。UDT组睾丸中AZIN2表达和精胺含量下调。然后，我们使用次黄嘌呤和黄嘌呤组合建立GC - 1细胞损伤模型。在该模型中，AZIN2表达和精胺含量下调。当用si - Azin2转染GC - 1细胞时，细胞活力和增殖能力下降。然而，在用过表达Azin2质粒转染的GC - 1细胞损伤模型中，AZIN2表达和精胺含量上调，逆转了次黄嘌呤和黄嘌呤引起的细胞损伤，并恢复了GC - 1细胞的增殖能力。这些结果表明，在隐睾中，AZIN2表达下调是睾丸损伤的一个因素。对AZIN2与生殖细胞之间联系的探讨具有重要的临床意义，因为它为隐睾的诊断和治疗提供了重要参考。
