Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation
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The role of the glucocorticoid receptor (GR) in glucocorticoid physiology and during development was investigated by generation of GR-deficient mice by gene targeting. GR -/- mice die within a few hours after birth because of respiratory failure. The lungs at birth are severely atelectatic, and development is impaired from day 15.5 p.c. Newborn livers have a reduced capacity to activate genes for key gluconeogenic enzymes. Feedback regulation via the hypothalamic-pituitary-adrenal axis is severely impaired resulting in elevated levels of plasma adrenocorticotrophic hormone (15-fold) and plasma corticosterone (2.5-fold). Accordingly, adrenal glands are enlarged because of hypertrophy of the cortex, resulting in increased expression of key cortical steroid biosynthetic enzymes, such as side-chain cleavage enzyme, steroid 11 beta-hydroxylase, and aldosterone synthase. Adrenal glands lack a central medulla and synthesize no adrenaline. They contain no adrenergic chromaffin cells and only scattered noradrenergic chromaffin cells even when analyzed from the earliest stages of medulla development. These results suggest that the adrenal medulla may be formed from two different cell populations: adrenergic-specific cells that require glucocorticoids for proliferation and/or survival, and a smaller noradrenergic population that differentiates normally in the absence of glucocorticoid signaling.
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GR-knockout mice have disordered hepatic gluconeogenesis and absent adrenomedullary chromaffin cells and die from neonatal respiratory distress syndrome.
“GR-knockout mice have disordered hepatic gluconeogenesis and absent adrenomedullary chromaffin cells and die from neonatal respiratory distress syndrome (639).”
From The Molecular Biology, Biochemistry, and Physiology of Human Steroidogenesis and Its Disorders (2011) · cites this paper as [639]
The sections on hepatic gluconeogenic enzymes and acute respiratory distress report impaired activation of gluconeogenic genes and death of nearly all GR-knockout mice within hours of birth after severe respiratory distress. But the section on chromaffin-cell development explicitly identifies scattered chromaffin cells in their adrenal glands: adrenergic cells are absent, not all adrenomedullary chromaffin cells. The indexed copy provides no page numbers for these sections. (LLM, conf=0.92)
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Steroid Hormone Biosynthesis and Actions in the Materno Fetoplacental Unit
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Familial/sporadic glucocorticoid resistance: clinical phenotype and molecular mechanisms
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- Authors
- Cole, T. J., Blendy, J. A., Monaghan, A. P., Krieglstein, K., Schmid, W., Aguzzi, A., Fantuzzi, G., Hummler, E., Unsicker, K., & Schütz, G.
- Affiliations
- German Cancer Research Center (DE)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1995-07-01
- Volume
- 9
- Issue
- 13
- Pages
- 1608-1621
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2068246413
- Cited by
- 946
- References
- 57
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 16 · 2023: 17 · 2022: 12 · 2021: 19 · 2020: 26 · 2019: 24 · 2018: 28 · 2017: 25 · 2016: 30 · 2015: 31 · 2014: 33 · 2013: 36 · 2012: 31
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- University of Washington
- Deutsche Forschungsgemeinschaft (SFB229)
- Leibniz-Gemeinschaft
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Keywords
- glucocorticoid receptor, lung maturation, atelectasis, hypothalamic-pituitary-adrenal axis, ACTH, corticosterone, adrenal cortex hypertrophy, steroidogenesis, gluconeogenesis
- MeSH terms
- Adrenal Cortex, Adrenal Medulla, Animals, Animals, Newborn, Cell Line, Corticosterone, Embryo, Mammalian, Epinephrine, Exons, Female, Heterozygote, Humans, Hypertrophy, Infant, Newborn, Lung, Male, Mice, Mutant Strains, Pregnancy, Receptors, Glucocorticoid, Recombination, Genetic, Reference Values, Respiratory Distress Syndrome, Newborn, Stem Cells, Restriction Mapping, Signal Transduction, In Situ Hybridization, Mice
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