CEDIE   05498
CENTRO DE INVESTIGACIONES ENDOCRINOLOGICAS "DR. CESAR BERGADA"
Unidad Ejecutora - UE
artículos
Título:
Physiologic Androgen Insensitivity of the fetal, neonatal and early infantile human testis is explained by the ontogeny of the androgen receptor expression in Sertoli cells
Autor/es:
CHEMES, HE; REY, R; NISTAL, M.; REGADERA, J.; MUSSE, M.; GONZÁLEZ-PERAMATO, P.; SERRANO, A.
Revista:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
Editorial:
The Endocrine Society
Referencias:
Año: 2008 vol. 93 p. 4408 - 4412
ISSN:
0021-972X
Resumen:
Context: Although gonadotropins and testosterone are high in the fetal/early postnatal periods, Sertoli cells remain immature and spermatogenesis does not progress. We hypothesized that Sertoli cells do not respond to testosterone because they do not express the androgen receptor. Objective: To describe the precise ontogeny of androgen receptor expression in the human testis from fetal life through adulthood. Design: Immunohistochemical study on testicular biopsies from fetal, neonatal, prepubertal, pubertal and adult human testes. Main outcome measures: Quantification of androgen receptor expression in Sertoli cells. Evaluation of AR expression in peritubular and interstitial cells, as well as of anti-Müllerian hormone and Inhibin-a was also performed. Results: Androgen receptor expression was first observed in the nuclei of few Sertoli cells at the age of 5 months. Labeling was weak in 2-15 % of Sertoli cells until 4 yr of age, and progressively increased thereafter. High levels of androgen receptor expression were observed in > 90 % from the age of 8 yr through adulthood. AR was positive in peritubular cells, and variable in interstitial cells. AMH immunolabeling was strong in all Sertoli cells from fetal life throughout prepuberty, and weakened progressively as spermatogenesis developed. Inhibin-a expression was detected in all Sertoli cells from fetal life through adulthood. Conclusions: A lack of androgen receptor expression could explain a physiologic Sertoli cell androgen insensitivity during fetal and early postnatal life, which may serve to protect the testis from precocious Sertoli cell maturation resulting in proliferation arrest and spermatogenic development.