Glucocorticoid action in development

Brown, Roger

doi:10.1097/01.med.0000162081.03216.e0

Cited by 7 publications

(5 citation statements)

References 65 publications

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“…Although glucocorticoids are often considered "housekeeping" hormones because of their roles in regulation of basal metabolism of all cells, they are now recognized as having critical developmental roles in many tissues (7). In our microarray study (1), Gene Ontology analysis revealed that only 14 of the 66 upregulated transcripts were in the "metabolism" category.…”

Section: Discussionmentioning

confidence: 98%

Diverse patterns of cell-specific gene expression in response to glucocorticoid in the developing small intestine

Yaylaoglu¹,

Agbemafle²,

Oesterreicher³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Although glucocorticoids are known to elicit functional maturation of the gastrointestinal tract, the molecular mechanisms of glucocorticoid action on the developing intestine have not been fully elucidated. Our previous microarray studies identified 66 transcripts as being rapidly induced in the jejunum following dexamethasone (Dex) administration to suckling mice. Now we report the specific cellular location of a subset of these transcripts. Mouse pups at P8 received Dex or vehicle and intestinal segments were collected 3-4 h later. Robotic-based in situ hybridization (ISH) was performed with digoxygenin-labeled riboprobes. Transcripts studied included Ndrg1, Sgk1, Fos, and two unknown genes (Gene 9 and Gene 36). As predicted, ISH revealed marked diversity of cellular expression. In small intestinal segments, Sgk1 mRNA was in all epithelial cells; Fos mRNA was confined to epithelial cells at the villus tip; and Ndrg1 and Gene 36 mRNAs were localized to epithelial cells of the upper crypt and villus base. The remaining transcript (Gene 9) was induced modestly in villus stroma and strongly in the muscle layers. In the colon, Ndrg1, Sgk1, and Gene 36 were induced in all epithelial cells; Gene 9 was in muscle layers only; and Fos was not detectable. For jejunal segments, quantitation of ISH signals in tissue from Dex-treated and vehicle-treated mice demonstrated mRNA increases very similar to those measured by Northern blotting. We conclude that glucocorticoid action in the intestine reflects diverse molecular mechanisms operating in different cell types and that quantitative ISH is a valuable tool for studying hormone action in this tissue.

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Section: Discussionmentioning

confidence: 98%

Diverse patterns of cell-specific gene expression in response to glucocorticoid in the developing small intestine

Yaylaoglu¹,

Agbemafle²,

Oesterreicher³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Similarly, 11-HSD1 is little expressed in the fetus during most of gestation [68]. It becomes expressed close to birth, notably in the liver and lung [68,70], where it contributes to the maturational effects of glucocorticoids that occur just prior to birth [71]. 11-HSD1 is also expressed at term in the chorion and the amnion, the fetal membranes that together comprise the amniotic sac [52,46,72].…”

Section: -Hsd2 Expression In the Feto-placental Unitmentioning

confidence: 99%

Antenatal endogenous and exogenous glucocorticoids and their impact on immune ontogeny and long-term immunity

et al. 2016

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Endogenous levels of glucocorticoids rise during pregnancy to warrant development and maturation of the fetal organs close to birth. However, during most of the gestation, the fetus is protected from excessive biologically active endogenous glucocorticoids by placental and fetal expression of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). Maternal stress, which may overwhelm placental 11β-HSD2 activity with high glucocorticoid levels, or administration of synthetic glucocorticoids to improve the survival chances of the premature newborn, are associated to postnatal increased risk for immune diseases. Fetal exposure to excessive glucocorticoids may underlie this altered postnatal immunity. Here, we revise the role that placental and fetal 11β-HSD2, fetal glucocorticoid exposure, and programming of the offspring's the hypothalamic-pituitary-adrenal (HPA) axis play on concerted steps in immune fetal development. We could identify gaps in knowledge about glucocorticoid-induced programming of immune diseases. Finally, based on current evidence about glucocorticoid and HPA axis-mediated immune regulation, we hypothesize on mechanisms that could drive the enhanced risk for atopies, infections, and type I diabetes in offspring that were prenatally exposed to glucocorticoids.

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“…In contrast, mice which lack MR survive birth, but die in the first 2 weeks of life of circulatory failure caused by renal salt-wasting (Berger et al 1996, Bleich et al 1999. Both GR and MR are expressed in the foetal heart (Brown et al 2005) and while MR appears to play a detrimental role in adult cardiac remodelling (Messaoudi et al 2012), how both receptors influence cardiac development and maturation remains poorly understood. GR is certainly present in the human heart from 12 weeks of gestation (Ballard & Ballard 1974) and in mouse heart from as early as embryonic (E) day E10.5, though it is not activated by endogenous glucocorticoids until E15.5 (Rog-Zielinska et al 2013).…”

Section: Glucocorticoid Receptorsmentioning

confidence: 99%

Glucocorticoids and foetal heart maturation; implications for prematurity and foetal programming

Rog-Zielinska¹,

Richardson²,

Denvir³

et al. 2013

Journal of Molecular Endocrinology

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Glucocorticoids are steroid hormones, essential in mammals to prepare for life after birth. Blood levels of glucocorticoids (cortisol in most mammals including humans; corticosterone in rats and mice) rise dramatically shortly before birth. This is mimicked clinically in the routine administration of synthetic glucocorticoids to pregnant women threatened by a preterm birth or to preterm infants to improve neonatal survival. Whilst effects on lung are well documented and essential for postnatal survival, those on heart are less well known. In this study, we review recent evidence for a crucial role of glucocorticoids in late gestational heart maturation. Either insufficient or excessive glucocorticoid exposure before birth may alter the normal glucocorticoid-regulated trajectory of heart maturation with potential life-long consequences.

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Glucocorticoid action in development

Cited by 7 publications

References 65 publications

Diverse patterns of cell-specific gene expression in response to glucocorticoid in the developing small intestine

Diverse patterns of cell-specific gene expression in response to glucocorticoid in the developing small intestine

Antenatal endogenous and exogenous glucocorticoids and their impact on immune ontogeny and long-term immunity

Glucocorticoids and foetal heart maturation; implications for prematurity and foetal programming

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