ArticleDevelopmental cell2016
An FGFR1-SPRY2 Signaling Axis Limits Basal Cell Proliferation in the Steady-State Airway Epithelium.
Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Fibroblast Growth Factors in Lung Development and Regeneration: Mechanisms and Therapeutic Potential.Cells · 2025Review
- A map of signaling responses in the human airway epithelium.Cell systems · 2024Article
- DNA methylation-mediatedFrontiers in molecular biosciences · 2024Article
- Review
- Exploiting the potential of lung stem cells to develop pro-regenerative therapies.Biology open · 2022Review
- Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Roles of airway basal stem cells in lung homeostasis and regenerative medicine.Respiratory research · 2022Review
- SARS-CoV-2 Infection and Lung Regeneration.Clinical microbiology reviews · 2022Review
- miRNA-34b/c regulates mucus secretion in RSV-infected airway epithelial cells by targeting FGFR1.Journal of cellular and molecular medicine · 2021Article
- Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases.The Journal of experimental medicine · 2019Article
- Genome-wide effect of pulmonary airway epithelial cell-specificFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Non-lytic clearance of influenza B virus from infected cells preserves epithelial barrier function.Nature communications · 2019Article
- Article
- Fank1 and Jazf1 promote multiciliated cell differentiation in the mouse airway epithelium.Biology open · 2018Article
- Fgf10 Signaling in Lung Development, Homeostasis, Disease, and Repair After Injury.Frontiers in genetics · 2018Review
- FGFR2 is required for airway basal cell self-renewal and terminal differentiation.Development (Cambridge, England) · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The steady-state airway epithelium has a low rate of stem cell turnover but can nevertheless mount a rapid proliferative response following injury. This suggests a mechanism to restrain proliferation at steady state. One such mechanism has been identified in skeletal muscle in which pro-proliferative FGFR1 signaling is antagonized by SPRY1 to maintain satellite cell quiescence. Surprisingly, we found that deletion of Fgfr1 or Spry2 in basal cells of the adult mouse trachea caused an increase in steady-state proliferation. We show that in airway basal cells, SPRY2 is post-translationally modified in response to FGFR1 signaling. This allows SPRY2 to inhibit intracellular signaling downstream of other receptor tyrosine kinases and restrain basal cell proliferation. An FGFR1-SPRY2 signaling axis has previously been characterized in cell lines in vitro. We now demonstrate an in vivo biological function of this interaction and thus identify an active signaling mechanism that maintains quiescence in the airway epithelium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.