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Pregnancy |
a Departments of Obstetrics and Gynaecology,
b Physiology,
c Pediatrics,
d Biochemistry,
e Anatomy and Cell Biology, CIHR Group in Fetal and Neonatal Health and Development, Child Health Research Institute, and Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada N6A 4V2
To gain insight into the role of 11ß-hydroxysteroid dehydrogenase (11ß-HSD) enzymes and actions of glucocorticoids in the murine placenta and uterus, the expression pattern of the mRNA for 11ß-HSD1 and 11ß-HSD2 and the glucocorticoid receptor (GR) protein were determined from Embryonic Day 12.5 (E12.5, term = E19) to E18.5 by in situ hybridization and immunohistochemistry, respectively. Consistent with its putative role in regulating the transplacental passage of maternal glucocorticoid to the fetus, 11ß-HSD2 mRNA was highly expressed in the labyrinthine zone (the major site of maternal/fetal exchange) at E12.5, and its level decreased dramatically at E16.5, when it became barely detectable. Remarkably, the silencing of 11ß-HSD2 gene expression coincided with the onset of 11ß-HSD1 gene expression in the labyrinth at E16.5 when moderate levels of 11ß-HSD1 mRNA were detected and maintained to E18.5. By contrast, neither 11ß-HSD1 mRNA nor 11ß-HSD2 mRNA were detected in any cell types within the basal zone from E12.5 to E18.5. Moreover, the expression of 11ß-HSD1 and 11ß-HSD2 in the decidua exhibited a high degree of cell specificity in that the mRNA for both 11ß-HSD1 and 11ß-HSD2 was detected in the decidua-stroma but not in the compact decidua. A distinct pattern was also observed within the endometrium where the mRNA for 11ß-HSD1 was expressed in the epithelium, whereas that for 11ß-HSD2 was confined strictly to the stroma. By comparison, the expression of GR in the placenta and uterus was ubiquitous and unremarkable throughout late pregnancy. In conclusion, the present study demonstrates for the first time remarkable spatial and temporal patterns of expression of 11ß-HSD1 and 11ß-HSD2 and GR in the murine placenta and uterus and highlights the intricate control of not only transplacental passage of maternal glucocorticoid to the fetus but also local glucocorticoid action during late pregnancy.
2 Correspondence: K. Yang, Lawson Health Research Institute, 268 Grosvenor Street, London, ON, Canada N6A 4V2. FAX: 519 646 6110; kyang{at}uwo.ca
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