The long and short of the prolactin receptor: the corpus luteum needs them both!
The long and short of the prolactin receptor: the corpus luteum needs them both!
复制标题
催乳素受体的长和短：黄体都需要它们！
DOI：
10.1095/biolreprod.111.098293
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发表时间：
2012
影响因子：
3.6
通讯作者：
Stocco,Carlos
中科院分区：
文献类型：
--
作者：
Stocco,Carlos
It is well known that prolactin is essential for the formation and maintenance of the corpus luteum in rodents. Prolactin secretion induced by mating transforms the corpus luteum of the cycle, a structure of limited functionality, into the corpus luteum of pregnancy, an endocrine gland that remains active throughout gestation, secreting sufficient progesterone to maintain uterine function [1]. What remains controversial is how prolactin interacts with the various types of cells that form the corpus luteum, leading to the initiation of luteal survival and developmental programs. This controversy was fueled by the finding that two major forms of the prolactin receptor are expressed from the same gene. Splicing of the initial transcript of this gene produces a long and a short form of the receptor. These forms, while identical in their extracellular structure, differ in their intracellular domain length and sequence [2]. The contribution of each form of the prolactin receptor to the regulation of the corpus luteum has puzzled researchers for decades. Nevertheless, because long form receptor signaling is required for corpus luteum function [3] and because overexpression of the short form of the receptor cannot prevent the luteal failure induced by deletion of the prolactin receptor gene [4, 5], activation of the long form was thought to mediate the luteotropic effect of prolactin. Until now, this hypothesis has remained untested.In this month’s Biology of Reproduction, Le et al.[6] address this issue by expressing the long form of the receptor in prolactin receptor knockout mice, either ubiquitously or specifically in the corpus luteum. Strikingly, the expression of the long form in either manner is not enough to sustain luteal function. As seen in the full knockout, long form knock-in females ovulate normally but are infertile, although progesterone administration rescues pregnancy, suggestive of inadequate luteal function. This is intriguing because the functionality of the reintroduced receptor was demonstrated by the phosphorylation of STAT5, one of the main mediators of prolactin action in luteal cells [7]. The long form receptor also rescues estrogen receptor-a and luteinizing hormone receptor expression, two well-known targets of prolactin [8]; their expression is abolished in the prolactin receptor knockout mice. Moreover, CDKN1B (p27kip) and CEBPB (C/EBPb), two factors induced during luteinization [9, 10], are expressed in long form knockin animals treated with hCG. Thus, although follicular cells respond to prolactin and luteinizing hormone, luteinization
