ArticleEndocrinology2025
Pituitary-Targeted Knockout of Glucocorticoid Receptors Disrupts Growth Hormone Expression During Embryonic Development.
Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Consensus Pituitary Atlas, a scalable resource for annotation, novel marker discovery, and analyses in mouse pituitary gland research.Cell reports · 2026Article
- NR3C1 is required for normal somatotrope differentiation and Foxo1 expression in pituitary.Endocrinology · 2026Article
- Glucocorticoids in breast cancer: physiologic mechanisms and relationship to risk, survival, and treatment response.Frontiers in endocrinology · 2026Review
- ScRNAseq Analysis of Chicken Embryonic Pituitary Reveals Cell Heterogeneity and a Cell Type Coexpressing Gh and Pomc.Endocrinology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies have implicated glucocorticoids in the regulation of somatotroph differentiation. However, few studies have investigated a requirement for glucocorticoid receptors (GR) in this process. We hypothesized that GR is essential for the normal ontogeny of pituitary growth hormone (GH) during mouse embryonic development. Anterior pituitary cells were isolated from e12.5 to e13.5 mice and e11 chickens and cultured with or without corticosterone (CORT) in the absence or presence of ZK98299, a GR-specific antagonist. CORT induced GH mRNA expression in pituitary cells from both species, and this response was blocked by inclusion of the GR antagonist. Mouse embryos with pituitary-targeted knockout of GR were generated utilizing the cre-LoxP Recombinase system under control of the pituitary-specific alpha-glycoprotein subunit (αGSU) promoter. All cre-positive GR(-/-) embryos died at birth. Therefore, anterior pituitary, brain, heart, liver, and muscle tissues, were collected on embryonic days 17.5/18.5 for RNA isolation and RT-qPCR analysis. Cre mRNA expression was only found in the pituitary, and GR mRNA levels were significantly decreased in the pituitaries of GR(-/-) embryos. GH mRNA was significantly decreased in pituitary-targeted GR(-/-) knockout embryos in comparison to wild-type GR(+/+) embryos. Significant differences in expression of other pituitary hormones in GR(-/-) embryos were not observed, indicating that the effect of pituitary-targeted knockout of GR was restricted to disruption of GH gene expression. To our knowledge, this is the first report that homozygous GR knockout in the anterior pituitary gland in mice suppresses embryonic GH expression, confirming an essential role for GR signaling in the normal ontogeny of somatotrophs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.