Dhanasekaran N, Sheela Rani C S, Moudgal N R
Mol Cell Endocrinol. 1983 Nov;33(1):97-112. doi: 10.1016/0303-7207(83)90059-x.
The changes that occur during follicular growth and atresia in the lysosomal enzyme activities and in gonadotropin receptors of isolated granulosa cells were studied. At different intervals after an injection of PMSG to 21-day-old female rats, the granulosa cells (GC) were isolated and the total activity of cathepsin-D, a representative lysosomal enzyme, and FSH receptor activity in terms of binding of [125I]oFSH to GC and the steroidogenic response of GC to FSH in vitro were determined. During the period of both follicular growth and atresia there was an inverse correlation between the lysosomal enzyme activity and FSH receptor activity of granulosa cells, the former being low during follicular growth or tropic phase when the levels of FSH receptors were increasing. During the atretic phase, beyond 48 h of PMSG treatment (perhaps due to the normal metabolic clearance of the injected PMSG), the cathepsin-D activity showed a significant increase while the FSH receptors were on the decline. That lack of the hormone was responsible for atresia was confirmed when an antiserum to PMSG was injected during the tropic phase (24 h after PMSG); this resulted in a sharp increase in cathepsin-D activity. Injection of excess amounts of either FSH or LH, along with or soon after PMSG antiserum, was found to prevent the increase in cathepsin-D activity, and also resulted in the maintenance of gonadotropin receptors. This suggested that gonadotropins can 'rescue' follicles from undergoing atresia. In the unprimed immature rat FSH, but not LH or hCG, mimicked the effects of PMSG, in terms of bringing about a reduction in cathepsin-D activity of GC. Also in such rats, neutralization of endogenous FSH with an antiserum to FSH resulted in an increase in the cathepsin-D activity of GC, suggesting that even the prepubertal rat ovary is dependent on the tropic support of FSH for prevention of atresia.
研究了分离的颗粒细胞在卵泡生长和闭锁过程中溶酶体酶活性及促性腺激素受体的变化。给21日龄雌性大鼠注射孕马血清促性腺激素（PMSG）后，在不同时间间隔分离颗粒细胞（GC），测定组织蛋白酶-D（一种代表性的溶酶体酶）的总活性、[125I]oFSH与GC结合方面的促卵泡激素（FSH）受体活性以及GC在体外对FSH的类固醇生成反应。在卵泡生长和闭锁期间，颗粒细胞的溶酶体酶活性与FSH受体活性呈负相关，在卵泡生长或促性腺阶段，当FSH受体水平升高时，前者较低。在闭锁阶段，PMSG处理48小时后（可能由于注射的PMSG正常代谢清除），组织蛋白酶-D活性显著增加，而FSH受体则在下降。当在促性腺阶段（PMSG后24小时）注射PMSG抗血清时，证实缺乏激素是闭锁的原因；这导致组织蛋白酶-D活性急剧增加。发现与PMSG抗血清一起或在其之后不久注射过量的FSH或促黄体生成素（LH）可防止组织蛋白酶-D活性增加，还能维持促性腺激素受体。这表明促性腺激素可以“挽救”卵泡免于闭锁。在未预处理的未成熟大鼠中，就降低GC的组织蛋白酶-D活性而言，FSH而非LH或人绒毛膜促性腺激素（hCG）模拟了PMSG的作用。同样在这类大鼠中，用FSH抗血清中和内源性FSH会导致GC的组织蛋白酶-D活性增加，这表明即使是青春期前大鼠的卵巢也依赖FSH的促性腺支持来预防闭锁。
