Journal
REPRODUCTIVE SCIENCES
Volume 24, Issue 1, Pages 57-66Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1933719116649696
Keywords
17-estradiol; GPR30; Src; PI3K; Akt; Sertoli cell
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Funding
- National Natural Science Foundation of China [31072183, 31101872]
- Major State Basic Research Development Program [2014CB138502]
- Fundamental Research Funds for the Central Universities [XDJK2014D030]
- Chongqing Postgraduate Innovation Program [CYB14056]
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Sertoli cell (SC) is a key element in the process of spermatogenesis. Accumulating research show that estrogen plays an important role in regulating boar SC proliferation. However, it is unclear whether phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/Akt) is involved in this process. In the present study, the role of PI3K/Akt on the 17-estradiol-induced piglet SC proliferation was explored. In addition, we also explained the roles of G-protein-coupled estrogen receptor (GPR30) and Sarcoma protein (Src) in this process. Our study demonstrated that, 17-estradiol induced activation of PI3K in a time-dependent manner. Both G-15 (an antagonist of GPR30, 0.1 mol/L) and PP2 (an inhibitor of Src, 2.0 mol/L) inhibited 17-estradiol-induced activation of PI3K, reduced SC proliferation, and decreased messenger RNA (mRNA) and protein expression of S-phase kinase-associated protein 2 (Skp2). We also found that 17-estradiol induced activation of Akt in a time-dependent manner. Both LY294002 (an inhibitor of PI3K) and 10-DEBC (an inhibitor of Akt) significantly reduced 17-estradiol-induced SC proliferation and reduced mRNA and protein expression of Skp2. In addition, LY294002 inhibited 17-estradiol-induced activation of Akt. The results indicated that 17-estradiol regulates SC proliferation by activating PI3K/Akt. Both GPR30 and Src are involved in 17-estradiol-induced phosphorylation of PI3K/Akt. Activation of PI3K/Akt enhances the expression of Skp2, which promotes SC proliferation.
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