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人子宫内膜中的催乳素及其受体。

Prolactin and its receptor in human endometrium.

作者信息

Tseng L, Mazella J

机构信息

Department of Obstetrics, Gynecology and Reproductive Medicine, State University of New York at Stony Brook 11794, USA.

出版信息

Semin Reprod Endocrinol. 1999;17(1):23-7. doi: 10.1055/s-2007-1016208.

DOI:10.1055/s-2007-1016208
PMID:10406072
Abstract

Synthesis of prolactin (PRL) in human endometrium extends from the late luteal phase of the menstrual cycle throughout the pregnancy. We have studied the hormonal requirements for the sustained production of PRL and its receptor (PRL-R) in a long-term primary cell culture system. Progestin stimulates the production PRL and its receptor when stromal cells transform into decidual cells. The rise in PRL production rate correlates with an increase in steady-state PRL mRNA levels which are caused by increased transcription rate gene. Replacing progestin by the antiprogestin, RU 486, causes a transient superinduction of PRL production followed by reduction to basal level of expression. On the other hand, RU 486 exerts immediate inhibition of PRL-receptor mRNA expression. In addition, relaxin (RLX) enhances PRL synthesis. The transcription of the PRL gene in endometrium is dependent upon the promotor 6-kb upstream of the transcription start site in the pituitary. That biological functions of PRL and its receptor are critical to implantation and the maintenance of pregnancy is suggested by the impaired fertility of PRL and PRL-R knockout mice. PRL enhances endometrial cell growth at low concentrations and inhibits it at high concentrations. This dual action indicates an autocrine action of PRL-R-mediated signaling transduction pathways during reproductive cycles and pregnancy. During gestation, decidual-derived prolactin regulates the volume of amniotic and fetal extracellular fluid and electrolytes.

摘要

人子宫内膜中催乳素(PRL)的合成从月经周期的黄体晚期开始,贯穿整个孕期。我们在长期原代细胞培养系统中研究了PRL及其受体(PRL-R)持续产生的激素需求。当基质细胞转化为蜕膜细胞时,孕激素刺激PRL及其受体的产生。PRL产生率的上升与稳态PRL mRNA水平的增加相关,这是由基因转录速率增加引起的。用抗孕激素RU 486替代孕激素会导致PRL产生的短暂超诱导,随后降至基础表达水平。另一方面,RU 486对PRL受体mRNA表达有即时抑制作用。此外,松弛素(RLX)增强PRL的合成。子宫内膜中PRL基因的转录依赖于垂体中转录起始位点上游6 kb的启动子。PRL及其受体基因敲除小鼠的生育能力受损,提示PRL及其受体的生物学功能对着床和维持妊娠至关重要。低浓度时PRL促进子宫内膜细胞生长,高浓度时则抑制。这种双重作用表明在生殖周期和孕期PRL-R介导的信号转导途径存在自分泌作用。在妊娠期,蜕膜来源的催乳素调节羊水和胎儿细胞外液及电解质的量。

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