Borgers Mareike, Wolter Martin, Hentrich Anna, Bergmann Martin, Stammler Angelika, Konrad Lutz
Department of Obstetrics and GynecologyMedical Faculty, Feulgenstraße 12, D-35392 Giessen, GermanyInstitute of Veterinary-Anatomy-Histology and -Embryology, Frankfurter Straße 98, D-35392 Giessen, Germany.
Department of Obstetrics and GynecologyMedical Faculty, Feulgenstraße 12, D-35392 Giessen, GermanyInstitute of Veterinary-Anatomy-Histology and -Embryology, Frankfurter Straße 98, D-35392 Giessen, Germany
Reproduction. 2014 Sep;148(3):315-20. doi: 10.1530/REP-14-0279. Epub 2014 Jul 1.
Disturbances of checkpoints in distinct stages of spermatogenesis (mitosis, meiosis, and spermiogenesis) contribute to impaired spermatogenesis; however, the efficiency of meiotic entry has not been investigated in more detail. In this study, we analyzed azoospermic patients with defined spermatogenic defects by the use of octamer-binding protein 2 for type A spermatogonia, sarcoma antigen 1 for mitosis-meiosis transition and SMAD3 for pachytene spermatocytes. Especially patients with maturation arrest (MA) at the level of primary spermatocytes showed significantly reduced numbers of spermatogonia compared with patients with histologically intact spermatogenesis or patients with hypospermatogenesis (Hyp). For a detailed individual classification of the patients, we distinguished between 'high efficiency of meiotic entry' (high numbers of pachytene spermatocytes) and 'low efficiency of meiotic entry' (low numbers of pachytene spermatocytes). Only patients with histologically normal spermatogenesis (Nsp) and patients with Hyp showed normal numbers of spermatogonia and a high efficiency of meiotic entry. Of note, only patients with histologically Nsp or patients with Hyp could compensate low numbers of spermatogonia with a high efficiency of meiotic entry. In contrast, patients with MA always showed a low efficiency of meiotic entry. This is the first report on patients with impaired spermatogenesis, showing that half of the patients with Hyp but all patients with MA cannot compensate reduced numbers in spermatogonia with a highly efficient meiosis. Thus, we suggest that compensatory meiosis mechanisms in human spermatogenesis exist.
精子发生不同阶段（有丝分裂、减数分裂和精子形成）的检查点紊乱会导致精子发生受损；然而，减数分裂起始的效率尚未得到更详细的研究。在本研究中，我们通过使用针对A型精原细胞的八聚体结合蛋白2、针对有丝分裂-减数分裂转变的肉瘤抗原1和针对粗线期精母细胞的SMAD3，分析了患有明确精子发生缺陷的无精子症患者。特别是与组织学上精子发生完整的患者或精子发生低下（Hyp）的患者相比，原发性精母细胞水平出现成熟停滞（MA）的患者精原细胞数量显著减少。为了对患者进行详细的个体分类，我们区分了“减数分裂起始高效率”（粗线期精母细胞数量多）和“减数分裂起始低效率”（粗线期精母细胞数量少）。只有组织学上精子发生正常（Nsp）的患者和Hyp患者显示精原细胞数量正常且减数分裂起始效率高。值得注意的是，只有组织学上Nsp的患者或Hyp患者能够通过减数分裂起始高效率来补偿精原细胞数量少的情况。相比之下，MA患者总是表现出减数分裂起始效率低。这是关于精子发生受损患者的首份报告，表明一半的Hyp患者但所有MA患者都无法通过高效减数分裂来补偿精原细胞数量的减少。因此，我们认为人类精子发生中存在补偿性减数分裂机制。
