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The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development

The prepartum surge in plasma cortisol concentrations in humans and sheep promotes fetal lung and surfactant system maturation in the support of air breathing after birth. This physiological process has been used to enhance lung maturation in the preterm fetus using maternal administration of betame...

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Autores principales: McGillick, Erin V, Orgeig, Sandra, McMillen, I Caroline, Morrison, Janna L
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3871449/
https://www.ncbi.nlm.nih.gov/pubmed/24400136
http://dx.doi.org/10.1002/phy2.130
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author McGillick, Erin V
Orgeig, Sandra
McMillen, I Caroline
Morrison, Janna L
author_facet McGillick, Erin V
Orgeig, Sandra
McMillen, I Caroline
Morrison, Janna L
author_sort McGillick, Erin V
collection PubMed
description The prepartum surge in plasma cortisol concentrations in humans and sheep promotes fetal lung and surfactant system maturation in the support of air breathing after birth. This physiological process has been used to enhance lung maturation in the preterm fetus using maternal administration of betamethasone in the clinical setting in fetuses as young as 24 weeks gestation (term = 40 weeks). Here, we have investigated the impact of fetal intravenous cortisol infusion during the canalicular phase of lung development (from 109- to 116-days gestation, term = 150 ± 3 days) on the expression of genes regulating glucocorticoid (GC) activity, lung liquid reabsorption, and surfactant maturation in the very preterm sheep fetus and compared this to their expression near term. Cortisol infusion had no impact on mRNA expression of the corticosteroid receptors (GC receptor and mineralocorticoid receptor) or HSD11B-2, however, there was increased expression of HSD11B-1 in the fetal lung. Despite this, cortisol infusion had no effect on the expression of genes involved in lung sodium (epithelial sodium channel -α, -β, or -γ subunits and sodium–potassium ATPase-β1 subunit) or water (aquaporin 1, 3, and 5) reabsorption when compared to the level of expression during exposure to the normal prepartum cortisol surge. Furthermore, in comparison to late gestation, cortisol infusion does not increase mRNA expression of surfactant proteins (SFTP-A, -B, and -C) or the number of SFTP-B-positive cells present in the alveolar epithelium, the cells that produce pulmonary surfactant. These data suggest that there may be an age before which the lung is unable to respond biochemically to an increase in fetal plasma cortisol concentrations.
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spelling pubmed-38714492014-01-07 The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development McGillick, Erin V Orgeig, Sandra McMillen, I Caroline Morrison, Janna L Physiol Rep Original Research The prepartum surge in plasma cortisol concentrations in humans and sheep promotes fetal lung and surfactant system maturation in the support of air breathing after birth. This physiological process has been used to enhance lung maturation in the preterm fetus using maternal administration of betamethasone in the clinical setting in fetuses as young as 24 weeks gestation (term = 40 weeks). Here, we have investigated the impact of fetal intravenous cortisol infusion during the canalicular phase of lung development (from 109- to 116-days gestation, term = 150 ± 3 days) on the expression of genes regulating glucocorticoid (GC) activity, lung liquid reabsorption, and surfactant maturation in the very preterm sheep fetus and compared this to their expression near term. Cortisol infusion had no impact on mRNA expression of the corticosteroid receptors (GC receptor and mineralocorticoid receptor) or HSD11B-2, however, there was increased expression of HSD11B-1 in the fetal lung. Despite this, cortisol infusion had no effect on the expression of genes involved in lung sodium (epithelial sodium channel -α, -β, or -γ subunits and sodium–potassium ATPase-β1 subunit) or water (aquaporin 1, 3, and 5) reabsorption when compared to the level of expression during exposure to the normal prepartum cortisol surge. Furthermore, in comparison to late gestation, cortisol infusion does not increase mRNA expression of surfactant proteins (SFTP-A, -B, and -C) or the number of SFTP-B-positive cells present in the alveolar epithelium, the cells that produce pulmonary surfactant. These data suggest that there may be an age before which the lung is unable to respond biochemically to an increase in fetal plasma cortisol concentrations. Blackwell Publishing Ltd 2013-11 2013-11-11 /pmc/articles/PMC3871449/ /pubmed/24400136 http://dx.doi.org/10.1002/phy2.130 Text en © 2013 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
spellingShingle Original Research
McGillick, Erin V
Orgeig, Sandra
McMillen, I Caroline
Morrison, Janna L
The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title_full The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title_fullStr The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title_full_unstemmed The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title_short The fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
title_sort fetal sheep lung does not respond to cortisol infusion during the late canalicular phase of development
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3871449/
https://www.ncbi.nlm.nih.gov/pubmed/24400136
http://dx.doi.org/10.1002/phy2.130
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