PI3K/Akt Activated by GPR30 and Src Regulates 17β-Estradiol-Induced Cultured Immature Boar Sertoli Cells Proliferation.
作者： Wei-Rong Yang , Feng-Wei Zhu , Jiao-Jiao Zhang , Yi Wang , Jia-Hua Zhang
关键词:
摘要: Sertoli cell (SC) is a key element in the process of spermatogenesis. Accumulating research show that estrogen plays an important role regulating boar SC proliferation. However, it unclear whether phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/Akt) involved this process. In present study, PI3K/Akt on 17β-estradiol-induced piglet proliferation was explored. addition, we also explained roles G-protein-coupled receptor (GPR30) and Sarcoma protein (Src) Our study demonstrated that, 17β-estradiol induced activation PI3K time-dependent manner. Both G-15 (an antagonist GPR30, 0.1 μmol/L) PP2 inhibitor Src, 2.0 inhibited PI3K, reduced proliferation, decreased messenger RNA (mRNA) expression S-phase kinase-associated 2 (Skp2). We found Akt LY294002 PI3K) 10-DEBC Akt) significantly mRNA Skp2. Akt. The results indicated regulates by activating PI3K/Akt. GPR30 Src are phosphorylation Activation enhances Skp2, which promotes
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