Opposite Models of Expression of Androgen Receptor (AR) and Retinoic Acid Receptor-α (RAR-α) in the Onset of Male Germ Cell Development in Hormonally Manipulated Rats

ABSTRACT

Vitamin A together with testosterone (T) and FSH play an essential role in regulating spermatogenesis. Androgens and Vitamin A act through specific nuclear receptors: AR, retinoic acid receptors (RAR-α, β, γ). Present study aimed to investigate relationship between expression of RAR-α and AR in the initiation of spermatogenesis during puberty in conditions of neonatal hormonal manipulation.

Experimental model of neonatal treatment with diethylstilbestrol (DES), GnRH-antagonist, T was used. Immunostaining for RAR-α and AR; 121-point counting were applied. Absolute nuclear volume (ANV) was estimated for Sertoli (SC), germ cells (GC) and their subtypes. At onset of puberty (d18) over expression of RAR-α was evident in SCs after DES-10 but not GnRHa treatment. Co-administration of T+DES restored the normal pattern of weak immunoreactivity. An opposite model of expression was seen for AR—loss of expression after DES but not GnRHa application and recovery by T-therapy. Similar reduction was found for spermatogonial ANV in both groups, whereas ANV of spermatocytes (Sc) is reduced in greater extent by DES (10x) than GnRHa (6x). Preleptotene (Pl), leptotene (L) and zygotene (Z) stages was also more affected by DES than GnRHa. Sertoli cell support toward spermatocytes (Sc/SC ratio) was more affected by DES (4x decrease) than GnRHa (2x) and the same tendency is found for Pl/SC and L-Z/SC.

In conclusion, data suggest possible interplay between retinoid and androgen signaling in Sertoli cells in the differentiation of male germ cells. The anti-androgenic effect of estrogens on meiotic germ cells is probably mediated by augmentation of RAR- α expression.

Keywords:

• RAR-α
• AR
• androgens
• estrogens
• spermatogenesis