ArticleAmerican journal of respiratory cell and molecular biology2013
Transcription factor p63 regulates key genes and wound repair in human airway epithelial basal cells.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- Epigenetic de-repression of basal cell metaplasia in aging AT2 cells is a risk factor for idiopathic pulmonary fibrosis (IPF).bioRxiv : the preprint server for biology · 2026Article
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- Generation of a human vascularized 3D airway model replicating native mucosal heterogeneity.Frontiers in bioengineering and biotechnology · 2026Article
- SMARCA4 regulates inducible BRD4 genomic redistribution coupling intrinsic immunity and plasticity in epithelial injury-repair.Nucleic acids research · 2025Article
- A lentiviral toolkit to monitor airway epithelial cell differentiation using bioluminescence.American journal of physiology. Lung cellular and molecular physiology · 2024Article
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- The airway epithelium: an orchestrator of inflammation, a key structural barrier and a therapeutic target in severe asthma.The European respiratory journal · 2024Review
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- Development of a novel air-liquid interface airway tissue equivalent model for in vitro respiratory modeling studies.Scientific reports · 2023Article
- Type 2 inflammation drives an airway basal stem cell program through insulin receptor substrate signaling.The Journal of allergy and clinical immunology · 2023Article
- Mimicking acute airway tissue damage using femtosecond laser nanosurgery in airway organoids.Frontiers in cell and developmental biology · 2023Article
- SARS-CoV-2 particles promote airway epithelial differentiation and ciliation.Frontiers in bioengineering and biotechnology · 2023Article
- Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD.Frontiers in immunology · 2023Review
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- Integrated genomics approaches identify transcriptional mediators and epigenetic responses to Afghan desert particulate matter in small airway epithelial cells.Physiological genomics · 2022Article
- Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway.Cell death and differentiation · 2022Article
- Dysregulated Notch Signaling in the Airway Epithelium of Children with Wheeze.Journal of personalized medicine · 2021Article
- TP63 basal cells are indispensable during endoderm differentiation into proximal airway cells on acellular lung scaffolds.NPJ Regenerative medicine · 2021Article
- An NKX2-1Scientific reports · 2021Article
- A 'tad' of hope in the fight against airway disease.Biochemical Society transactions · 2020Review
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The airway epithelium in asthma displays altered repair and incomplete barrier formation. Basal cells are the progenitor cells of the airway epithelium, and can repopulate other cell types after injury. We previously reported increased numbers of basal cells expressing the transcription factor p63 in the airway epithelium of patients with asthma. Here we sought to determine the molecular consequences of p63 expression in basal human airway epithelial cells during wound repair. Because at least six isoforms of p63 exist (N-terminally truncated [ΔN] versus transcriptional activation promoter variants and α, β, or γ 3' splice variants), the expression of all isoforms was investigated in primary human airway epithelial cells (pHAECs). We modulated p63 expression, using small interfering RNA (siRNA) and adenoviral constructs to determine the effects of p63 on 21 candidate target genes by RT-PCR, and on repair using a scratch wound assay. We found that basal pHAECs from asthmatic and nonasthmatic donors predominantly expressed the N-terminally truncated p63α variant (ΔNp63α) isoform, with no disease-specific differences in expression. The knockdown of ΔNp63, using specific siRNA, decreased the expression of 11 out of 21 genes associated with epithelial repair and differentiation, including β-catenin, epidermal growth factor receptor, and Jagged1. The loss of ΔNp63 significantly inhibited wound closure (which was associated with the decreased expression of β-catenin and Jagged1), reduced epithelial proliferation as measured by Ki-67 staining, and increased E-cadherin expression, potentially preventing cytokinesis. In conclusion, ΔNp63α is the major isoform expressed in basal pHAECs, and is essential for epithelial wound repair. The role of ΔNp63α in epithelial barrier integrity requires further study to understand its role in health and disease.
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