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Distinct roles for SOX2 and SOX21 in differentiation, distribution and maturation of pulmonary neuroendocrine cells

Evelien Eenjes, Anne Boerema-de Munck, Marjon Buscop-van Kempen, Dick Tibboel, View ORCID ProfileRobbert J. Rottier
doi: https://doi.org/10.1101/2022.01.18.476762
Evelien Eenjes
1Department of Pediatric Surgery, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands
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Anne Boerema-de Munck
1Department of Pediatric Surgery, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands
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Marjon Buscop-van Kempen
1Department of Pediatric Surgery, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands
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Dick Tibboel
1Department of Pediatric Surgery, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands
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Robbert J. Rottier
1Department of Pediatric Surgery, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands
2Department of Cell Biology, Erasmus Medical Center, Rotterdam, The Netherlands
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  • ORCID record for Robbert J. Rottier
  • For correspondence: r.rottier@erasmusmc.nl
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ABSTRACT

Pulmonary neuroendocrine (NE) cells represent a small population in the airway epithelium, but despite this, hyperplasia of NE cells is associated with several lung diseases, such as congenital diaphragmatic hernia and bronchopulmonary dysplasia. The molecular mechanisms causing the development of NE cell hyperplasia remains poorly understood. Previously, we showed that the SOX21 modulates the SOX2-initiated differentiation of epithelial cells in the airways (Eenjes, 2021). Here, we show that precursor NE cells start to develop in the SOX2+SOX21+ airway region and that SOX21 suppresses the differentiation of airway progenitors to precursor NE cells. During development, clusters of NE cells start to form and NE cells mature by expressing neuropeptide proteins, such as CGRP. Deficiency in SOX2 resulted in decreased clustering, while deficiency in SOX21 increased both the numbers of NE ASCL1+ precursor cells early in development, and the number of cell clusters at E18.5. In addition, at the end of gestation (E18.5), a number of NE cells in Sox2 heterozygous mice, did not yet express CGRP suggesting a delay in maturation. In conclusion, SOX2 and SOX21 function in the initiation, migration and maturation of NE cells.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted January 18, 2022.
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Distinct roles for SOX2 and SOX21 in differentiation, distribution and maturation of pulmonary neuroendocrine cells
Evelien Eenjes, Anne Boerema-de Munck, Marjon Buscop-van Kempen, Dick Tibboel, Robbert J. Rottier
bioRxiv 2022.01.18.476762; doi: https://doi.org/10.1101/2022.01.18.476762
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Distinct roles for SOX2 and SOX21 in differentiation, distribution and maturation of pulmonary neuroendocrine cells
Evelien Eenjes, Anne Boerema-de Munck, Marjon Buscop-van Kempen, Dick Tibboel, Robbert J. Rottier
bioRxiv 2022.01.18.476762; doi: https://doi.org/10.1101/2022.01.18.476762

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