Several lines of evidence support a key role of estradiol-17β (E2) in male fertility. We have used a non-mammalian vertebrate model, the frog Rana esculenta, to investigate the regulation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) activity in the testis during the annual sexual cycle and to study whether E2 exerts a role in spermatogenesis through the regulation of ERK1/2 activity. ERK1/2 proteins are present in the cytoplasm and nucleus of the primary and secondary spermatogonia (SPG), and in the nucleus of primary spermatocytes. The annual E2 profile shows a progressive increase during active spermatogenesis with a peak in the month of June. In parallel, ERK1/2 are highly phosphorylated during the period of active spermatogenesis (from April to July) compared with the regressive period (September/October) and winter stasis (from November to March). E2 treatment induces the proliferation of primary SPG, possibly via the activation of ERK1/2, and this effect is counteracted by the anti-estrogen ICI 182-780.
Estradiol-induced mitogen-activated protein kinase (extracellular signal-regulated kinase 1 and 2) activity in the frog (Rana esculenta) testis
CHIEFFI, Paolo;COLUCCI D'AMATO, Generoso Luca;FRANCO, Renato;
2000
Abstract
Several lines of evidence support a key role of estradiol-17β (E2) in male fertility. We have used a non-mammalian vertebrate model, the frog Rana esculenta, to investigate the regulation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) activity in the testis during the annual sexual cycle and to study whether E2 exerts a role in spermatogenesis through the regulation of ERK1/2 activity. ERK1/2 proteins are present in the cytoplasm and nucleus of the primary and secondary spermatogonia (SPG), and in the nucleus of primary spermatocytes. The annual E2 profile shows a progressive increase during active spermatogenesis with a peak in the month of June. In parallel, ERK1/2 are highly phosphorylated during the period of active spermatogenesis (from April to July) compared with the regressive period (September/October) and winter stasis (from November to March). E2 treatment induces the proliferation of primary SPG, possibly via the activation of ERK1/2, and this effect is counteracted by the anti-estrogen ICI 182-780.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.