Abstract：
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) control antral follicular growth by regulating several processes, such as the synthesis of hormones and signaling molecules, proliferation, survival, apoptosis, luteinization, and ovulation. To exert these effects, gonadotropins bind to their respective Gs protein-coupled receptors, activating the protein kinase A (PKA) pathway or recruiting Gq proteins to activate protein kinase C (PKC) signaling. Although the action mechanism of FSH and LH is clear, recently, it has been shown that both gonadotropins promote the synthesis of sphingosine-1-phosphate (S1P) in granulosa and theca cells through the activation of sphingosine kinase 1. Moreover, the inhibition of SPHKs reduces S1P synthesis, cell viability, and the proliferation of follicular cells in response to gonadotropins, and the addition of S1P to the culture medium increases the proliferation of granulosa and theca cells without apparent effects on sexual steroid synthesis. Therefore, we consider that S1P is a crucial signaling molecule that complements the canonical gonadotropin pathway to promote the proliferation and viability of granulosa and theca cells.
摘要：
卵泡刺激素（FSH）和黄体生成素（LH）通过调节几个过程来控制窦卵泡的生长，比如激素和信号分子的合成，扩散,生存,凋亡，黄体化，和排卵。为了发挥这些作用，促性腺激素与它们各自的Gs蛋白偶联受体结合，激活蛋白激酶A（PKA）途径或募集Gq蛋白以激活蛋白激酶C（PKC）信号。虽然FSH和LH的作用机制是明确的，最近,已经表明，两种促性腺激素通过激活鞘氨醇激酶1促进颗粒细胞和卵泡膜细胞中1-磷酸鞘氨醇（S1P）的合成。此外，抑制SPHKs减少S1P合成，细胞活力，以及卵泡细胞对促性腺激素的反应增殖，在培养基中添加S1P可增加颗粒细胞和卵泡膜细胞的增殖，而对性类固醇的合成没有明显影响。因此,我们认为S1P是一个重要的信号分子，它补充了经典的促性腺激素途径，以促进颗粒细胞和卵泡膜细胞的增殖和活力。
