17β-Estradiol Regulates Cultured Immature Boar Sertoli Cell Proliferation via the cAMP-ERK1/2 Pathway and the Estrogen Receptor β

Estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells via the estrogen receptor β (ERβ) and the cAMP-extracellular signal-regulated kinase (ERK1/2) pathway. Low levels (10−10−10−8 mol L−1) of 17β-estradiol increased cell number, but high levels (10−7−10−6 mol L−1) decreased it (P < 0.05). Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol (10−6 mol L−1) (P > 0.05). The effects of 17β-estradiol (10−9 mol L−1) peaked at the first 24 h (P < 0.05). 17β-estradiol activated ERK1/2 from 5 min to 24 h, but the activiy of ERK1/2 began to decrease after 4 h. Both PD98059 and U0126, two ERK inhibitors, blocked cell division (P < 0.05). 17β-estradiol (10−10−10−6 mol L−1) dose-dependently increased cAMP production (P < 0.05), and both 17β-estradiol (10−9 mol L−1) and forskolin, which increases cAMP levels, induced cell proliferation and activated ERK1/2 (P < 0.05). Rp-cAMP, an antagonist of cAMP, blocked this 17β-estradiol activity (P < 0.05). Two estrogen receptor antagonists, ICI 182780 and ERβ antagonist (ERβAnt), reduced Sertoli cell number, cAMP production and ERK1/2 activation (P < 0.05), but ERaAnt did not (P > 0.05). Therefore, 17β-estradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.