ArticleThe Journal of biological chemistry2003
Down-regulation of retinoic acid receptor alpha signaling is required for sacculation and type I cell formation in the developing lung.
Article in The Journal of biological chemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 60 citations in OpenAlex.
- Transmural pressure signals through retinoic acid to regulate lung branching.Development (Cambridge, England) · 2022Article
- Review
- Changes of DNA methylation are associated with changes in lung function during adolescence.Respiratory research · 2020Article
- Cyp26b1 is an essential regulator of distal airway epithelial differentiation during lung development.Development (Cambridge, England) · 2020Article
- Retinoic Acid: A Key Regulator of Lung Development.Biomolecules · 2020Review
- Modulation of retinoid signaling: therapeutic opportunities in organ fibrosis and repair.Pharmacology & therapeutics · 2020Review
- RARα and RARγ reciprocally control K5Organogenesis · 2017Article
- Association between nuclear expression of retinoic acid receptor alpha and beta and clinicopathological features and prognosis of advanced non-small cell lung cancer.International journal of clinical oncology · 2016Article
- Combined antenatal therapy with retinoic acid and tracheal occlusion in a rat model of congenital diaphragmatic hernia.Pediatric surgery international · 2016Article
- HDAC3-Dependent Epigenetic Pathway Controls Lung Alveolar Epithelial Cell Remodeling and Spreading via miR-17-92 and TGF-β Signaling Regulation.Developmental cell · 2016Article
- Neuroendocrine factors regulate retinoic acid receptors in normal and hypoplastic lung development.The Journal of physiology · 2015Article
- Efficient generation of lung and airway epithelial cells from human pluripotent stem cells.Nature biotechnology · 2014Article
- Deletion of STK40 protein in mice causes respiratory failure and death at birth.The Journal of biological chemistry · 2013Article
- Development and remodeling of the vertebrate blood-gas barrier.BioMed research international · 2013Review
- Retinol and retinyl palmitate in foetal lung mice: sexual dimorphism.Critical care research and practice · 2013Article
- Article
- Comparative molecular developmental aspects of the mammalian- and the avian lungs, and the insectan tracheal system by branching morphogenesis: recent advances and future directions.Frontiers in zoology · 2012Article
- Maternal smoking and the retinoid pathway in the developing lung.Respiratory research · 2012Article
- Emerging roles for retinoids in regeneration and differentiation in normal and disease states.Biochimica et biophysica acta · 2012Review
- Vitamin A in reproduction and development.Nutrients · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Although retinoic acid (RA) has been shown to be critical for lung development, little is known about when RA is required and the role of individual RA receptors (RAR) in this process. Previously reported data from an RA responsive element RARE-lacZ reporter mouse show that when epithelial tubules are branching and differentiating RA signaling becomes markedly down-regulated in the epithelium. It is unclear why this down-regulation occurs and what role it might play in the developing lung. Here we analyze the effects of preventing potential progenitors of the distal lung from turning off RA signaling by locally expressing constitutively activated RARalpha or RARbeta chimeric receptors (RARVP16) in branching airways of transgenic mice. Continued RA activation resulted in lung immaturity in both cases, but the phenotypes were remarkably different. RARalphaVP16 lungs did not expand to form saccules or morphologically identifiable type I cells. High levels of surfactant protein C (Sp-C), thyroid transcription factor-1 (Ttf1), and Gata6, but not Sp-A or Sp-B in the epithelium at birth suggested that in these lungs differentiation was arrested at an early stage. These alterations were not observed in RARbetaVP16 lungs, which showed relatively less severe changes. Our data suggest a model in which activation of RAR signaling at the onset of lung development establishes an initial program that assigns distal cell fate to the prospective lung epithelium. Down-regulation of RA signaling, however, is required to allow completion of later steps of this differentiation program that ultimately form mature type I and II cells.
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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.