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Noggin regulates foregut progenitor cell programming, and misexpression leads to esophageal atresia
Carolina Pinzon-Guzman, … , Scott D. Boden, James R. Goldenring
Carolina Pinzon-Guzman, … , Scott D. Boden, James R. Goldenring
Published May 19, 2020
Citation Information: J Clin Invest. 2020;130(8):4396-4410. https://doi.org/10.1172/JCI123597.
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Noggin regulates foregut progenitor cell programming, and misexpression leads to esophageal atresia

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.

Authors

Carolina Pinzon-Guzman, Sreedhara Sangadala, Katherine M. Riera, Evgenya Y. Popova, Elizabeth Manning, Won Jae Huh, Matthew S. Alexander, Julia S. Shelton, Scott D. Boden, James R. Goldenring

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