التفاصيل البيبلوغرافية
| العنوان: |
Noggin regulates foregut progenitor cell programming, and misexpression leads to esophageal atresia. |
| المؤلفون: |
Pinzon-Guzman, Carolina1 carolina.pinzon-guzman@vumc.org, Sangadala, Sreedhara2, Riera, Katherine M.1, Popova, Evgenya Y.3, Manning, Elizabeth1, Won Jae Huh4, Alexander, Matthew S.5, Shelton, Julia S.6, Boden, Scott D.2, Goldenring, James R.1,7,8,9, Huh, Won Jae4 (AUTHOR) |
| المصدر: |
Journal of Clinical Investigation. Aug2020, Vol. 130 Issue 8, p4396-4410. 15p. |
| مصطلحات موضوعية: |
*FOREGUT, *PROGENITOR cells, *ESOPHAGUS, *HUMAN abnormalities, *ANIMAL experimentation, *BIOLOGICAL models, *CARRIER proteins, *CELL differentiation, *CELL lines, *COMPARATIVE studies, *GENES, *RESEARCH methodology, *MEDICAL cooperation, *MICE, *RESEARCH, *STEM cells, *TISSUES, *EVALUATION research, ESOPHAGEAL atresia |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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