Hadziselimovic Faruk, Gegenschatz-Schmid Katharina, Verkauskas Gilvydas, Docampo-Garcia Maria J, Demougin Philippe, Bilius Vytautas, Malcius Dalius, Dasevicius Darius, Stadtler Michael B
Sex Dev. 2016;10(3):136-46. doi: 10.1159/000447762. Epub 2016 Sep 13.
The whole genome RNA profiling of testicular biopsies by DNA strand-specific RNA sequencing was examined to determine a potential causative role of isolated congenital cryptorchidism in azoospermia and/or infertility in the context of our previously published GeneChip data. Cryptorchid patients, aged 7 months to 5 years and otherwise healthy, were enrolled in this prospective study. During surgery, testicular tissue biopsies were obtained for histological examination and RNA sequencing. Fifteen patients were selected based on the histological results and were divided into 2 groups. Seven were classified as belonging to the high infertility risk (HIR) and 8 to the low infertility risk (LIR) group. Cryptorchid boys in the HIR group lacked transformation of gonocytes into Ad spermatogonia due to impaired mini-puberty. This group of patients will be infertile despite successful surgery. The new important finding was a decreased PROK2, CHD7, FGFR1, and SPRY4 gene expression in the HIR group. Furthermore, identification of multiple differences in gene expression between HIR and LIR groups underscores the importance of an intact hypothalamic-pituitary-gonadal axis for fertility development. Our RNA profiling data strongly support the theory that in the HIR group of cryptorchid boys insufficient PROK2/CHD7/FGFR1/SPRY4 gene expression induces deficient LH secretion, resulting in impaired mini-puberty and infertility. We therefore recommend hormonal treatment for this cohort of cryptorchid boys with defective mini-puberty following a seemingly successful orchidopexy.
通过DNA链特异性RNA测序对睾丸活检组织进行全基因组RNA分析,以确定在我们之前发表的基因芯片数据背景下,孤立性先天性隐睾症在无精子症和/或不育症中的潜在致病作用。年龄在7个月至5岁且无其他健康问题的隐睾症患者被纳入这项前瞻性研究。在手术过程中,获取睾丸组织活检样本用于组织学检查和RNA测序。根据组织学结果选择了15名患者,并将其分为两组。7名被归类为高不育风险(HIR)组,8名被归类为低不育风险(LIR)组。HIR组的隐睾症男孩由于青春期前发育受损,生殖母细胞无法转化为Ad精原细胞。尽管手术成功,这组患者仍将不育。新的重要发现是HIR组中PROK2、CHD7、FGFR1和SPR的基因表达降低。此外,HIR组和LIR组之间基因表达的多重差异表明,完整的下丘脑-垂体-性腺轴对生育能力发展至关重要。我们的RNA分析数据有力地支持了这样一种理论,即在HIR组的隐睾症男孩中,PROK2/CHD7/FGFR1/SPR基因表达不足会导致促黄体生成素分泌不足,从而导致青春期前发育受损和不育。因此,我们建议对这组青春期前发育缺陷的隐睾症男孩在看似成功的睾丸固定术后进行激素治疗。