ArticleAmerican journal of respiratory cell and molecular biology2008
Glucocorticoid regulation of human pulmonary surfactant protein-B mRNA stability involves the 3'-untranslated region.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Systemic corticosteroids for severe community-acquired pneumonia: a narrative review of mechanisms and critical appraisal of recent trials in ICU.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Molecular Levels?International journal of molecular sciences · 2021Review
- A primate-specific RNA-binding protein (RBMXL3) is involved in glucocorticoid regulation of human pulmonary surfactant protein B (SP-B) mRNA stability.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Expression of surfactant protein B is dependent on cell density in H441 lung epithelial cells.PloS one · 2017Article
- Glucocorticoid regulation of lung development: lessons learned from conditional GR knockout mice.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Sequences of a hairpin structure in the 3'-untranslated region mediate regulation of human pulmonary surfactant protein B mRNA stability.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Advances in tryptophan hydroxylase-2 gene expression regulation: new insights into serotonin-stress interaction and clinical implications.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012Review
- Glucocorticoid regulation of human pulmonary surfactant protein-B (SP-B) mRNA stability is independent of activated glucocorticoid receptor.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Transient pretreatment with glucocorticoid ablates innate toxicity of systemically delivered adenoviral vectors without reducing efficacy.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of pulmonary surfactant, a complex mixture of lipids and proteins that acts to reduce alveolar surface tension, is developmentally regulated and restricted to lung alveolar type II cells. The hydrophobic protein surfactant protein-B (SP-B) is essential in surfactant function, and insufficient levels of SP-B result in severe respiratory dysfunction. Glucocorticoids accelerate fetal lung maturity and surfactant synthesis both experimentally and clinically. Glucocorticoids act transcriptionally and post-transcriptionally to increase steady-state levels of human SP-B mRNA; however, the mechanism(s) by which glucocorticoids act post-transcriptionally is unknown. We hypothesized that glucocorticoids act post-transcriptionally to increase SP-B mRNA stability via sequence-specific mRNA-protein interactions. We found that glucocorticoids increase SP-B mRNA stability in isolated human type II cells and in nonpulmonary cells, but do not alter mouse SP-B mRNA stability in a mouse type II cell line. Deletion analysis of an artificially-expressed SP-B mRNA indicates that the SP-B mRNA 3'-untranslated region (UTR) is necessary for stabilization, and the region involved can be restricted to a 126-nucleotide-long region near the SP-B coding sequence. RNA electrophoretic mobility shift assays indicate that cytosolic proteins bind to this region in the absence or presence of glucocorticoids. The formation of mRNA:protein complexes is not seen in other regions of the SP-B mRNA 3'-UTR. These results indicate that a specific 126-nucleotide region of human SP-B 3'-UTR is necessary for increased SP-B mRNA stability by glucocorticoids by a mechanism that is not lung cell specific and may involve mRNA-protein interactions.
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Registered trials
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