Human Reproduction, Vol. 14, No. 1, 136-143,
January 1999
© 1999 European Society of Human Reproduction and Embryology
Reversion of the differentiated phenotype and maturation block in Sertoli cells in pathological human testis
1 Institute of Anatomy and Cell Biology, University of Halle (Saale), Germany, 2 Unité de Recherches sur l'Endocrinologie du Développement (INSERM), Ecole Normale Supérieure, Département de Biologie, Montrouge, France, 3 Department of Urology, University of Münster, Germany, 4 Institute of Reproductive Medicine, University of Münster, Germany, 5 Children's Hospital, University of Leipzig, Germany, 6 Department of Pathology, The Toronto Hospital, Toronto, Ontario, Canada, 7 Banting and Best Department of Medical Research, University of Toronto, Toronto, Ontario, Canada, 8 Centro de Investigaciones Endocrinológicas, Hospital de Niflos, Buenos Aires, Argentina and 9 Institute of Veterinary Anatomy, University of Giessen, Germany
To study the relationship between abnormal Sertoli cell differentiation and spermatogenic impairment, we examined the expression of Sertoli cell markers normally lost at puberty, cytokeratin 18 (CK18), anti-Müllerian hormone (AMH) and M2A antigen, in three children (aged 1–2 years), 50 adults (aged 19–45 years) with obstructive or non-obstructive azoospermia or oligozoospermia, and six patients (aged 1–18 years) with 5
-reductase deficiency. There was CK18 and/or AMH expression, but never M2A antigen expression, associated with spermatogonial arrest or Sertoli cell-only (SCO) syndrome in infertile men. Loss of M2A antigen suggests the transition of Sertoli cells to an adult phenotype, while CK18 and/or AMH expression may be a manifestation of de-differentiation of Sertoli cells. In 5-reductase deficiency, there was a sequential loss of CK18, M2A antigen and AMH around puberty, associated with partial spermatogenesis. The persistence of immature Sertoli cells expressing M2A antigen was associated with prepubertal seminiferous cords and SCO syndrome. Therefore, 5-reductase deficiency may prevent the maturation of Sertoli cells, resulting in impairment of spermatogenesis, and loss of M2A antigen expression coincides with a critical step in the Sertoli cell maturation. High follicle stimulating hormone concentrations due to failure of normal Sertoli cell differentiation indicate a normal development pattern of the hypothalamic–pituitary–gonadal axis.
Key words:
anti-Müllerian hormone/cytokeratin/male infertility/M2A antigen/5-reductase deficiency
10 To whom correspondence should be addressed at: Institut für Anatomie und Zellbiologie Große Steinstraße 52, D-06097 Halle (Saale), Germany
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