Freeman D A, Ascoli M
Proc Natl Acad Sci U S A. 1982 Dec;79(24):7796-800. doi: 10.1073/pnas.79.24.7796.
We have reported previously that the human choriogonadotropin (hCG) receptors of cultured Leydig tumor cells can be down-regulated with hCG or mouse epidermal growth factor (mEGF) and that such down-regulation results in a loss of the steroidogenic response of the cells to hCG. Exposure of the cells to hCG, but not to mEGF, also resulted in a decrease in steroidogenic responses to cholera toxin and cAMP. The results presented herein show that the hCG-induced loss of steroidogenic response to cAMP is due to the depletion of intracellular cholesterol and that this depletion can be prevented by the addition of low density lipoprotein. Our results also show that after exposure of the cells to mEGF or hCG their steroidogenic response to hCG is limited by the number of hCG receptors, regardless of the presence of low density lipoprotein.
我们之前曾报道,培养的睾丸间质细胞瘤细胞的人绒毛膜促性腺激素(hCG)受体可被hCG或小鼠表皮生长因子(mEGF)下调,且这种下调导致细胞对hCG的类固醇生成反应丧失。将细胞暴露于hCG而非mEGF,也会导致对霍乱毒素和cAMP的类固醇生成反应降低。本文给出的结果表明,hCG诱导的对cAMP类固醇生成反应丧失是由于细胞内胆固醇耗竭,且这种耗竭可通过添加低密度脂蛋白来预防。我们的结果还表明,细胞暴露于mEGF或hCG后,它们对hCG的类固醇生成反应受hCG受体数量限制,无论低密度脂蛋白是否存在。