Fetal development of Leydig cell activity in the mouse is independent of pituitary gonadotroph function
Fetal development of Leydig cell activity in the mouse is independent of pituitary gonadotroph function
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DOI：
10.1210/en.139.3.1141
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发表时间：
1998-03-01
期刊：
影响因子：
4.8
通讯作者：
Huhtaniemi, I
中科院分区：
文献类型：
--
作者：
O'Shaughnessy, PJ;Baker, P;Huhtaniemi, I
在胎儿发育期间，睾丸分泌抗苗勒管激素和睾酮以诱导雄性表型的形成。成年Leydig细胞在LH的控制下分泌睾酮，但胎儿垂体在调节胎儿Leydig细胞功能中的作用尚不清楚。为了研究垂体和间质细胞功能之间的早期关系，我们研究了正常小鼠和缺乏GnRH和循环促性腺激素的性腺功能减退（hpg）小鼠的胎儿垂体LH水平和间质细胞功能的发育。在正常和hpg小鼠，垂体LH含量几乎检测不到，直到胚胎第17天（E17），当水平开始显着增加，在两组。然而，hpg小鼠的LH水平在所有年龄段仅为正常水平的约10%。全长LH受体转录本首次检测到胎儿睾丸E16在正常和hpg小鼠。在正常小鼠中，编码细胞色素P450侧链裂解和17 α-羟化酶的睾丸信使RNA（mRNA）水平从E13开始增加，在出生前后达到峰值。在hpg小鼠中，编码这些酶的mRNA水平在出生前都是正常的，但在出生时出现了显著下降。睾丸mRNA编码3 β-羟类固醇脱氢酶I型的水平在正常和hpg小鼠中相似，在发育过程中几乎没有变化。正常动物睾丸内睾酮在E18达到高峰，出生后再次下降。在hpg小鼠中，睾丸内睾酮水平在整个胎儿发育过程中和出生当天都是正常的，但在纳塔尔后第5天几乎检测不到。结果表明：1）在缺乏内源性循环促性腺激素的情况下，小鼠胎儿间质细胞功能正常; 2）出生后不久，间质细胞开始依赖促性腺激素; 3）在缺乏GnRH的情况下，垂体LH合成可以开始，但正常合成和分泌水平依赖于LH。
During fetal development the testes secrete anti-Mullerian hormone and testosterone to induce formation of the male phenotype. Adult Leydig cells secrete testosterone under the control of LH, but the role of the fetal pituitary in regulating fetal Leydig cell function is unclear. To study the early relationship between pituitary and Leydig cell function, we have examined the development of fetal pituitary LH levels and Leydig cell function in normal mice and in hypogonadal (hpg) mice that lack GnRH and, thus, circulating gonadotropins. In normal and hpg mice, pituitary LH content was barely detectable until embryonic day 17 (E17), when levels began to increase significantly in both groups. Pituitary levels of LH in hpg mice were, however, only about 10% of normal at all ages. Full-length LH receptor transcripts were first detectable in fetal testes on E16 in both normal and hpg mice. In normal mice, levels of testicular messenger RNA (mRNA) encoding cytochrome P450 side-chain cleavage and 17 alpha-hydroxylase increased from E13 to reach a peak around birth. In hpg mice, levels of mRNA encoding these enzymes were normal until around birth, at which time there was a significant decline. Levels of testicular mRNA encoding 3 beta-hydroxysteroid dehydrogenase type I were similar in normal and hpg mice and showed little change during development. Intratesticular testosterone reached a peak on E18 in normal animals before declining again after birth. In hpg mice, intratesticular testosterone levels were normal throughout fetal development and on the day of birth, but were barely detectable by post natal day 5. Results show 1) that fetal Leydig cell function in the mouse is normal in the absence of endogenous circulating gonadotropins; 2) that Leydig cells become dependent on gonadotropins shortly after birth; and 3) that pituitary LH synthesis can start in the absence of GnRH but is dependent on LH for a normal level of synthesis and secretion.