17β-Estradiol Regulates Cultured Immature Boar Sertoli Cell Proliferation via the cAMP-ERK1/2 Pathwa

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 ERαAnt did not(P > 0.05).Therefore,17βestradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.