Fetoplacental Hormones and Human Gestation

Diczfalusy, E.

doi:10.1007/978-1-4684-2892-6_26

Cited by 3 publications

(3 citation statements)

References 84 publications

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“…By contrast, Burton demonstrated that fetal mouse liver had the capacity to convert 11-dehydrocorticosterone to corticosterone [6,7], setting a precedent for the local tissue activation of glucocorticoids in specific fetal tissues. The discovery by Liggins that glucocorticoids stimulate fetal lung development and reduce the morbidity and mortality of preterm birth catalyzed the then burgeoning interest in fetal steroid metabolism [8]. The presence of 11b HSD 1 activity in human fetal lung cells was first reported by Smith, Torday and Giroud in 1973 [9].…”

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confidence: 99%

The Physiologic Significance of 11beta-hydroxysteroid Dehydrogenase Type 1 in Fetal Lung Development Redux

Torday

2005

Horm Metab Res

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Hundertmark et al. [1] recently reported that 11-oxo steroids, like their 11-hydroxy isoforms, can stimulate fetal lung maturation due to the expression of 11b-hydroxysteroid dehydrogenase Type 1 (11b HSD 1), the enzyme that converts (inactive) cortisone to (active) cortisol [2]. In a subsequent study, this group has shown that knocking out the 11b HSD 1 gene inhibits lung maturation and surfactant synthesis [3], confirming the biological significance of 11b HSD 1 in lung development. A series of studies performed by my collaborators and myself beginning more than 30 years ago had previously demonstrated the biological activity and significance of 11b HSD 1 in fetal human, rabbit and rat lung development. These studies were the first to elucidate the physiologic role of glucocorticoids in normal fetal lung development [4]. I would like to relate these studies, which were overlooked in the Hundertmark publications.Our laboratory at McGill University was the first to discover why the placenta is a`barrier' to steroids. Hillman and Giroud [5] demonstrated that the placenta quantitatively oxidizes cortisol to cortisone as it passes through from mother to fetus. This was thought to be protective since glucocorticoids are classically considered to be catabolic. By contrast, Burton demonstrated that fetal mouse liver had the capacity to convert 11-dehydrocorticosterone to corticosterone [6,7], setting a precedent for the local tissue activation of glucocorticoids in specific fetal tissues. The discovery by Liggins that glucocorticoids stimulate fetal lung development and reduce the morbidity and mortality of preterm birth catalyzed the then burgeoning interest in fetal steroid metabolism [8]. The presence of 11b HSD 1 activity in human fetal lung cells was first reported by Smith, Torday and Giroud in 1973 [9]. In a subsequent study [10], we showed that cortisol could directly affect fetal rabbit lung cell surfactant phospholipid synthesis, and that cortisol stimulated 11b HSD 1 activity by fetal rabbit lung cells [11]. To determine whether 11b HSD 1 could actively generate cortisol from cortisone in the intact fetal lung, we perfused fetal rabbit lung via the pulmonary artery with 3 H-cortisone, and demonstrated quantitative secretion of 3 H-cortisol from the pulmonary vein [12]; we also reported that 11b HSD 1 activity increased significantly from 23 to 29 days gestation (day 31 = term).The physiological significance of 11b HSD 1 activation by fetal lung fibroblasts was elucidated by in-depth studies on the cellmolecular mechanism of glucocorticoid action on lung maturation. Smith [13] discovered that cortisol stimulated lung fibroblast synthesis of a low molecular-weight paracrine factor he termed fibroblast-pneumonocyte factor (FPF), which was secreted into the extracellular milieu and stimulated surfactant phospholipid synthesis by the alveolar type II cell [14]. My laboratory pursued these observations by demonstrating that the hormonedependent sex difference in fetal lung development was due to the differential ...

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confidence: 99%

The Physiologic Significance of 11beta-hydroxysteroid Dehydrogenase Type 1 in Fetal Lung Development Redux

Torday

2005

Horm Metab Res

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“…During pregnancy, the placenta is the first temporary endocrine organ to develop from cells originating from the embryo [1]. The placenta produces several steroid hormones, including estrogen and progesterone, which are pivotal in the maintenance of healthy pregnancy [2]. The main role of the placenta is to anchor the conceptus; prevent maternal immune responses; and provide an interface to exchange nutrients, oxygen, and waste products [3].…”

Section: Placental Developmentmentioning

confidence: 99%

The TGFβ Family in Human Placental Development at the Fetal-Maternal Interface

2020

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Emerging data suggest that a trophoblast stem cell (TSC) population exists in the early human placenta. However, in vitro stem cell culture models are still in development and it remains under debate how well they reflect primary trophoblast (TB) cells. The absence of robust protocols to generate TSCs from humans has resulted in limited knowledge of the molecular mechanisms that regulate human placental development and TB lineage specification when compared to other human embryonic stem cells (hESCs). As placentation in mouse and human differ considerably, it is only with the development of human-based disease models using TSCs that we will be able to understand the various diseases caused by abnormal placentation in humans, such as preeclampsia. In this review, we summarize the knowledge on normal human placental development, the placental disease preeclampsia, and current stem cell model systems used to mimic TB differentiation. A special focus is given to the transforming growth factor-beta (TGFβ) family as it has been shown that the TGFβ family has an important role in human placental development and disease.

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“…These observations led Diczfalusy [168][169][170][171][172] to introduce the idea of a single endocrine steroidogenic unit of those two organs, the fetoplacental unit. Early studies revealed distinct variations in the pattern of steroidogenic enzyme distribution in fetal adrenal and placenta.…”

Section: The Fetoplacental Unitmentioning

confidence: 99%

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

Malendowicz

2011

Folia Histochem Cytobiol.

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Fetoplacental Hormones and Human Gestation

Cited by 3 publications

References 84 publications

The Physiologic Significance of 11beta-hydroxysteroid Dehydrogenase Type 1 in Fetal Lung Development Redux

The Physiologic Significance of 11beta-hydroxysteroid Dehydrogenase Type 1 in Fetal Lung Development Redux

The TGFβ Family in Human Placental Development at the Fetal-Maternal Interface

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

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