1. Noggin regulates foregut progenitor cell programming, and misexpression leads to esophageal atresia
- Author
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Pinzon-Guzman, Carolina, Sangadala, Sreedhara, Riera, Katherine M., Popova, Evgenya Y., Manning, Elizabeth, Huh, Won Jae, Alexander, Matthew S., Shelton, Julia S., Boden, Scott D., and Goldenring, James R.
- Subjects
Hyclone Laboratories Inc. ,Birth defects ,Health care industry - 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., Introduction Congenital esophageal atresia (EA) represents a failure of the esophagus to develop as a continuous passage, which causes the esophagus to end in a blind upper pouch rather than [...]
- Published
- 2020
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