Gegenschatz-Schmid Katharina, Verkauskas Gilvydas, Demougin Philippe, Bilius Vytautas, Dasevicius Darius, Stadler Michael B, Hadziselimovic Faruk
Cryptorchidism Research Institute, Kindermedizinisches Zentrum Liestal, 4410 Liestal, Switzerland.
Children's Surgery Centre, Faculty of Medicine, Vilnius of University, Vilnius 01513, Lithuania.
Genes (Basel). 2017 Oct 11;8(10):267. doi: 10.3390/genes8100267.
Defective mini-puberty results in insufficient testosterone secretion that impairs the differentiation of gonocytes into dark-type (Ad) spermatogonia. The differentiation of gonocytes into Ad spermatogonia can be induced by administration of the gonadotropin-releasing hormone agonist, GnRHa (Buserelin, INN)). Nothing is known about the mechanism that underlies successful GnRHa treatment in the germ cells. Using RNA-sequencing of testicular biopsies, we recently examined RNA profiles of testes with and without GnRHa treatment. Here, we focused on the expression patterns of known gene markers for gonocytes and spermatogonia, and found that , , BRACHYURY/, and were associated with defective mini-puberty and were responsive to GnRHa. These results indicate novel testosterone-dependent genes and provide valuable insight into the transcriptional response to both defective mini-puberty and curative GnRHa treatment, which prevents infertility in man with one or both undescended (cryptorchid) testes.
微小青春期缺陷会导致睾酮分泌不足，从而损害生殖母细胞向暗型（Ad）精原细胞的分化。给予促性腺激素释放激素激动剂（GnRHa，布舍瑞林，国际非专利药品名称）可诱导生殖母细胞分化为Ad精原细胞。目前对于GnRHa在生殖细胞中成功治疗的潜在机制尚不清楚。我们最近通过对睾丸活检组织进行RNA测序，研究了GnRHa治疗组和未治疗组睾丸的RNA图谱。在此，我们聚焦于生殖母细胞和精原细胞已知基因标志物的表达模式，发现 、 、短尾蛋白（BRACHYURY）/ 以及 与微小青春期缺陷相关且对GnRHa有反应。这些结果表明了新的睾酮依赖性基因，并为微小青春期缺陷和GnRHa治疗（可预防单侧或双侧隐睾男性不育）的转录反应提供了有价值的见解。
