© Springer International Publishing Switzerland 2014. Fetal glucocorticoid exposure is a key mechanism involved in adverse programming outcomes in the adult. Impairment of fetal growth has predominantly been attributed to direct effects of glucocorticoids on the fetus, prematurely shifting tissue development from a proliferative to a more functionally mature state. However, fetal growth is dependent on a complex interplay of maternal, placental, and fetal endocrine signals, and glucocorticoid-mediated fetal growth retardation is likely also to relate to disturbances in placental growth and function. Regulation of fetal glucocorticoid exposure is achieved by the placental glucocorticoid barrier, which involves glucocorticoid inactivation within the labyrinth zone of the murine placenta by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). Overexposure to glucocorticoids or depletion of 11β-HSD2 has a dramatic effect on placental development and function, with a reduction in capillary networks and alterations in nutrient transport. This work highlights the finding that adverse programming effects of glucocorticoids are not exclusively due to direct actions on the fetus but are also a consequence of changes in placental development and function.
|Journal||Research and Perspectives in Endocrine Interactions|
|Publication status||Published - 2014|