我们使用增殖原代培养未成熟大鼠睾丸间质细胞表达重组人促黄体激素 L /绒毛膜促性腺激素( CG )的受体( LHR )来测试假设激活这一受体会抑制细胞凋亡. 我们比较了LH/CG 与EGF 和IGF - 1 的影响,因为先前已表明,它们刺激睾丸间质细胞增殖和/或抑制凋亡. HGC ,EGF和IGF-I促进原代培养未成熟大鼠睾丸间质细胞的ERK1 / 2和AKT磷酸化.并且这三种激素有利于胸(腺嘧啶脱氧核)苷掺入和抑制药物诱导的细胞凋亡. 使用选择性抑制剂ERK1 / 2 ( UO126 )或Akt( LY294002 ) ,表明睾丸间质细胞依赖hCG和EGF的增殖都是与ERK1 / 2和AKT的参与有关,但只有ERK1 / 2作用时是抗凋亡的. 同样的策略表明,IGF - I的增殖和抗凋亡作用完全是由Akt通路介导的.这些结果表明,通过刺激的ERK1 / 2通路,激活LHR抑制睾丸间质细胞凋亡.

Activation of the Lutropin/Choriogonadotropin Receptor Inhibits Apoptosis of Immature Leydig Cells in Primary Culture
    We used proliferating primary cultures of immature rat Leydig cells expressing the recombinant human LH/choriogonadotropin (CG) receptor (LHR) to test the hypothesis that activation of this receptor inhibits apoptosis. We also compared the effects of LH/CG with epidermal growth factor (EGF) and IGF-I because these have been previously shown to stimulate proliferation and/or inhibit apoptosis in Leydig cells. Human CG (hCG), EGF, and IGF-I stimulated the phosphorylation of ERK1/2 and Akt in primary cultures of immature rat Leydig cells. These three hormones also robustly stimulated thymidine incorporation and inhibited drug-induced apoptosis. Using selective inhibitors of ERK1/2 (UO126) or Akt phosphorylation (LY294002), we show that the ERK1/2 and Akt cascades are both involved in the hCG- and EGF-dependent proliferation of Leydig cells, but only the ERK1/2 cascade is involved in their antiapoptotic actions. The same strategy showed that the proliferative and antiapoptotic actions of IGF-I are mediated entirely by the Akt pathway. These results show that activation of the LHR inhibits apoptosis in Leydig cells and that it does so through stimulation of the ERK1/2 pathway.

相关阅读:
深度测序揭示猪生殖腺miRNA转录组特征
睾丸激素影响手指长度
从小鼠睾丸中获得多功能干细胞的新方法
从男性睾丸中分离出干细胞
分离和鉴定人LYPD6一个ly-6家族新成员