ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Increased expression of senescence markers in cystic fibrosis airways.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- MLKL regulates intracellular trafficking of neutrophil elastase to promote lung epithelial cell senescence.American journal of respiratory cell and molecular biology · 2026Article
- The Role of Cellular Senescence in Obstructive Airway Diseases: From Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2026Review
- Ecological partitioning enables phage-antibiotic cooperation in a human Pseudomonas infection.Nature communications · 2026Article
- Exploring the uncharted role of cell senescence in rare diseases.Orphanet journal of rare diseases · 2025Review
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Managing an ageing cystic fibrosis population: challenges and priorities.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Wound repair and immune function in theFrontiers in cellular and infection microbiology · 2025Review
- Leukocyte telomere length and attrition in association with disease severity in cystic fibrosis patients.Aging · 2024Article
- Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- Article
- Discovery of dysregulated circular RNAs in whole blood transcriptomes from cystic fibrosis patients - implication of a role for cellular senescence in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023Article
- Senopathies-Diseases Associated with Cellular Senescence.Biomolecules · 2023Article
- Nutrition Interventions of Herbal Compounds on Cellular Senescence.Oxidative medicine and cellular longevity · 2022Review
- Involvement of MiRNA-211-5p and Arhgap11a Interaction During Osteogenic Differentiation of MC3T3-E1 Cells.Frontiers in surgery · 2022Article
- Neutrophil Elastase and Chronic Lung Disease.Biomolecules · 2021Review
- Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Leukocyte Telomere Length Is Not Reduced in Children and Adults with Cystic Fibrosis but Associates with Clinical Characteristics-A Cross-Sectional Study.Journal of clinical medicine · 2021Article
- Enhancing Cystic Fibrosis Immune Regulation.Frontiers in pharmacology · 2021Article
- Cystic Fibrosis Lung Disease in the Aging Population.Frontiers in pharmacology · 2021Review
- What Role Does CFTR Play in Development, Differentiation, Regeneration and Cancer?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cystic Fibrosis (CF) is a chronic lung disease characterized by chronic neutrophilic airway inflammation and increased levels of neutrophil elastase (NE) in the airways. We have previously reported that NE treatment triggers cell cycle arrest. Cell cycle arrest can lead to senescence, a complete loss of replicative capacity. Importantly, senescent cells can be proinflammatory and would perpetuate CF chronic inflammation. By immunohistochemistry, we evaluated whether airway sections from CF and control subjects expressed markers of senescence, including p16(INK4a) (p16), a cyclin-dependent kinase inhibitor, phospho-Histone H2A.X (γH2A.X), and phospho-checkpoint 2 kinase (phospho-Chk2), which are also DNA damage response markers. Compared with airway epithelium from control subjects, CF airway epithelium had increased levels of expression of all three senescence markers. We hypothesized that the high load of NE in the CF airway triggers epithelial senescence by upregulating expression of p16, which inhibits cyclin-dependent kinase 4 (CDK4). Normal human bronchial epithelial (NHBE) cells, cultured in air-liquid interface were treated with NE (0, 200, and 500 nM) to induce visible injury. Total cell lysates were collected and evaluated by Western analysis for p16 protein expression and CDK4 kinase activity. NE significantly increased p16 expression and decreased CDK4 kinase activity in NHBE cells. These results support the concept that NE triggers expression of senescence markers in CF airway epithelial cells.
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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.