CEDIE   05498
CENTRO DE INVESTIGACIONES ENDOCRINOLOGICAS "DR. CESAR BERGADA"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
CYP26B1 declines postnatally in Sertoli cells independently of androgen action in the mouse testis
Autor/es:
SCHTEINGART, HELENA F.; REY, RODOLFO A.; EDELSZTEIN, NADIA Y.
Lugar:
Ciudad de Buenos Aires
Reunión:
Congreso; X Reunión de la Sociedad Latinoamericana de Biología del Desarrollo; 2019
Institución organizadora:
Sociedad Latinoamericana de Biología del Desarrollo
Resumen:
In male mammals, meiosis begins at puberty and is androgen-dependent.Anomalies in androgen synthesis and action seen in human and mouse experimentalmodels showed the effect of the androgen rise at pubertal onset on AMHinhibition -marker for Sertoli cell maturation- and meiotic onset in thetestis. In the mouse, retinoic acid is also needed for meiotic onset in thetestis. CYP26B1 degrades retinoic acid in the testis during prenataldevelopment preventing meiosis initiation. Given the concurrence of meioticentry and Sertoli cell maturation in response to androgens at pubertal onset,we proposed that CYP26B1 is downregulated by androgens in the Sertoli cellduring puberty. By immunohistochemistry on sections of mouse testis fromdifferent ages we show that CYP26B1 expression decays in Sertoli cells afterbirth. However, luciferase reporter assays and RT-qPCR using the prepubertalmouse Sertoli cell line SMAT1 revealed no changes in Cyp26b1 expression in response to androgens. Furthermore, whenusing primary Sertoli cell cultures from 10-day-old mice we did not findchanges in Cyp26b1 or CYP26B1 levels in response to androgens, nor didwe find evidence for an interaction between the androgen receptor and regionsof the Cyp26b1 gene promoter by ChIP-qPCR. To sum up, the herebyreported postnatal decay in CYP26B1 expression in the Sertoli cell is not dueto a direct inhibitory effect of androgens in the mouse.