| Literature DB >> 32427591 |
Carolina Pinzon-Guzman1, Sreedhara Sangadala2, Katherine M Riera1, Evgenya Y Popova3, Elizabeth Manning1, Won Jae Huh4, Matthew S Alexander5, Julia S Shelton6, Scott D Boden2, James R Goldenring1,7,8,9.
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.Entities:
Keywords: Development; Embryonic development; Human stem cells; Surgery
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Year: 2020 PMID： 32427591 PMCID： PMC7410075 DOI： 10.1172/JCI123597
Source DB: PubMed Journal: J Clin Invest ISSN： 0021-9738 Impact factor: 14.808