ArticleCellular and molecular life sciences : CMLS2023
Distinct roles for SOX2 and SOX21 in differentiation, distribution and maturation of pulmonary neuroendocrine cells.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Interplay of the nasal microbiome and epigenome among adolescents.Clinical epigenetics · 2026Article
- Pulmonary neuroendocrine cells in pediatric asthma and bronchopulmonary dysplasia: neuroimmune-developmental mechanisms and translational implications.Frontiers in medicine · 2026Review
- Reinitiating lung development: a novel approach in the management of bronchopulmonary dysplasia.Respiratory research · 2024Review
- Descriptive and Functional Genomics in Neonatal Respiratory Distress Syndrome: From Lung Development to Targeted Therapies.International journal of molecular sciences · 2024Review
- SOX2 and SOX21 in Lung Epithelial Differentiation and Repair.International journal of molecular sciences · 2022Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
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. 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 mature 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.
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Registered trials
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