Prolactin receptor expression in the developing mouse embryo

SJ Tzeng, DIH Linzer - Molecular Reproduction and …, 1997 - Wiley Online Library
SJ Tzeng, DIH Linzer
Molecular Reproduction and Development: Incorporating Gamete Research, 1997Wiley Online Library
We have examined the developmental pattern of prolactin receptor expression in the mouse
by reverse transcription‐polymerase chain reaction, in situ hybridization, and radioligand
binding and have found two unexpected aspects of temporal regulation. First, high levels of
prolactin receptor mRNA were detected in mouse embryos at day 8 and day 18, but levels
decreased between these days to a minimum at∼ day 14. In contrast, placental prolactin
receptor mRNA levels remained constant throughout this gestational period. Second, on …
Abstract
We have examined the developmental pattern of prolactin receptor expression in the mouse by reverse transcription‐polymerase chain reaction, in situ hybridization, and radioligand binding and have found two unexpected aspects of temporal regulation. First, high levels of prolactin receptor mRNA were detected in mouse embryos at day 8 and day 18, but levels decreased between these days to a minimum at ∼day 14. In contrast, placental prolactin receptor mRNA levels remained constant throughout this gestational period. Second, on embryonic day 16 the mRNA encoding the long form of the prolactin receptor is more abundant in the fetal liver than any of the short receptor form mRNAs, but by day 18 a switch occurs and the mRNA encoding one of the short receptor forms becomes the predominant receptor mRNA in that tissue. Expression of the receptor mRNA and protein is widespread throughout the fetus, with especially high levels in developing bone and cartilagenous structures, the thymus and pituitary, the tongue and skeletal muscle, and certain regions of the brain. The pattern of expression of prolactin receptor in the fetal mouse suggests an important role for the placental lactogens, the major ligands for fetal prolactin receptors, in fetal growth and development. Mol. Reprod. Dev. 48:45–52, 1997. © 1997 Wiley‐Liss, Inc.
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