Changes in competence determine the timing of two sequential glucocorticoid effects on sympathoadrenal progenitors

Michelsohn, Arie M.; Anderson, David J.

doi:10.1016/0896-6273(92)90285-l

Cited by 97 publications

(63 citation statements)

References 56 publications

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“…These results seem to confirm those of Ross et al (11) who also reported that under Dex treatment neuroblastoma cells were assuming a chromaffinlike aspect. Even though we did not analyze whether these cells were also exhibiting some biochemical features of epithelial-like cells their general aspect could lead to this conclusion, in agreement with several in vitro and in vivo results suggesting that Gc may induce a transdifferentiation of neuroblastoma cells towards a chromaffin, epitheliallike phenotype (7,10,(12)(13)(14)(15). The results reported here indicate that RU486, while counteracting the effect of Dex on chemomigration, induced a modification of the morphology of the cells.…”

Section: Discussionsupporting

confidence: 53%

“…Several studies suggest that glucocorticoids (Gc) have a potent effect inducing the differentiation of neural crest cells towards the chromaffin cell type of the adrenal medulla (7,(10)(11)(12)(13)(14)(15). In addition, Gc influence a series of biochemical parameters of neuroblastoma cells that may further suggest a possible differentiation of these cells.…”

Section: La Casulari Et Almentioning

confidence: 99%

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Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

Casulari¹,

Dondi²,

Maggi³

et al. 2006

Braz J Med Biol Res

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Glucocorticoids (Gc) influence the differentiation of neural crestderived cells such as those composing sympathoadrenal tumors like pheochromocytomas, as well as neuroblastomas and gangliomas. In order to obtain further information on the effects of Gc on cells evolving from the neural crest, we have used the human neuroblastoma cell line SK-N-SH to analyze: 1) the presence and the binding characteristics of Gc receptors in these cells, 2) the effect of dexamethasone (Dex) on the migration of SK-N-SH cells, and 3) the effect of Dex on the organization of the cytoskeleton of SK-N-SH cells. We show that: 1) receptors that bind [ 3 H]-Dex with high affinity and high capacity (Kd of 9.6 nM, Bmax of 47 fmol/mg cytosolic protein, corresponding to 28,303 sites/cell) are present in cytosolic preparations of SK-N-SH cells, and 2) treatment with Dex (in the range of 10 nM to 1 µM) has an inhibitory effect (from 100% to 74 and 43%, respectively) on the chemotaxis of SK-N-SH cells elicited by fetal bovine serum. This inhibition is completely reversed by the Gc receptor antagonist RU486 (1 µM), and 3) as demonstrated by fluorescent phalloidin-actin detection, the effect of Dex (100 nM) on SK-N-SH cell migration is accompanied by modifications of the cytoskeleton organization that appear with stress fibers. These modifications did not take place in the presence of 1 µM RU486. The present data demonstrate for the first time that Dex affects the migration of neuroblastoma cells as well as their cytoskeleton organization by interacting with specific receptors. These findings provide new insights on the mechanism(s) of action of Gc on cells originating in the neural crest.

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Section: Discussionsupporting

confidence: 53%

Section: La Casulari Et Almentioning

confidence: 99%

Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

Casulari¹,

Dondi²,

Maggi³

et al. 2006

Braz J Med Biol Res

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“…The foetal heart is fully formed in both mice (wE13.5-E14.5) and humans (w40 days; indicated by vertical bars, top) before the glucocorticoid surge that occurs in the few days before birth in most mammals (Michelsohn & Anderson 1992, Fowden et al 1998, Henderson & Anderson 2009). In mice, the late gestational increase in foetal plasma corticosterone (triangles in the schematic representation above) is essential for maturation of the foetal heart (Rog-Zielinska et al 2013).…”

Section: Figurementioning

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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“…expression (11,12) and before fetal adrenal gland steroidogenesis starts (24)], and at E17.5 (as placental 11β-HSD2 falls, around peak fetal plasma glucocorticoid levels, and just before birth, typically E18.5 in Hsd11b2 +/− mice; ref. 10).…”

Section: Significancementioning

confidence: 99%

Pravastatin ameliorates placental vascular defects, fetal growth, and cardiac function in a model of glucocorticoid excess

Wyrwoll

Noble

Thomson

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Fetoplacental glucocorticoid overexposure is a significant mechanism underlying fetal growth restriction and the programming of adverse health outcomes in the adult. Placental glucocorticoid inactivation by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) plays a key role. We previously discovered that Hsd11b2 −/− mice, lacking 11β-HSD2, show marked underdevelopment of the placental vasculature. We now explore the consequences for fetal cardiovascular development and whether this is reversible. We studied Hsd11b2 +/+ , Hsd11b2 +/− , and Hsd11b2 −/− littermates from heterozygous (Hsd11b +/− ) matings at embryonic day (E)14.5 and E17.5, where all three genotypes were present to control for maternal effects. Using high-resolution ultrasound, we found that umbilical vein blood velocity in Hsd11b2 −/− fetuses did not undergo the normal gestational increase seen in Hsd11b2 +/+ littermates. Similarly, the resistance index in the umbilical artery did not show the normal gestational decline. Surprisingly, given that 11β-HSD2 absence is predicted to initiate early maturation, the E/A wave ratio was reduced at E17.5 in Hsd11b2 −/− fetuses, suggesting impaired cardiac function. Pravastatin administration from E6.5, which increases placental vascular endothelial growth factor A and, thus, vascularization, increased placental fetal capillary volume, ameliorated the aberrant umbilical cord velocity, normalized fetal weight, and improved the cardiac function of Hsd11b2 −/− fetuses. This improved cardiac function occurred despite persisting indications of increased glucocorticoid exposure in the Hsd11b2 −/− fetal heart. Thus, the pravastatin-induced enhancement of fetal capillaries within the placenta and the resultant hemodynamic changes correspond with restored fetal cardiac function. Statins may represent a useful therapeutic approach to intrauterine growth retardation due to placental vascular hypofunction.placenta | 11β-HSD2 | glucocorticoids | fetal heart | developmental programming

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Changes in competence determine the timing of two sequential glucocorticoid effects on sympathoadrenal progenitors

Cited by 97 publications

References 56 publications

Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

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

Pravastatin ameliorates placental vascular defects, fetal growth, and cardiac function in a model of glucocorticoid excess

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