Noggin regulates foregut progenitor cell programming, and misexpression leads to esophageal atresia.
basic_science · Level V
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- Record sourced from PubMed, PMID 32427591.
- Also identified by DOI 10.1172/JCI123597 and PMC identifier 7410075.
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Abstract
Esophageal atresia (EA/TEF) is a common congenital abnormality present in 1 of 4000 births. Here we show that atretic esophagi lack Noggin (NOG) expression, resulting in immature esophagus that contains respiratory glands. Moreover, when using mouse esophageal organoid units (EOUs) or tracheal organoid units (TOUs) as a model of foregut development and differentiation in vitro, NOG determines whether foregut progenitors differentiate toward esophageal or tracheal epithelium. These results indicate that NOG is a critical regulator of cell fate decisions between esophageal and pulmonary morphogenesis, and its lack of expression results in EA/TEF.
Medical subject headings
- Carrier Proteins
- Cell Differentiation
- Esophageal Atresia
- Gene Expression Regulation, Developmental
- Models, Biological
- Stem Cells