ArticleAmerican journal of respiratory and critical care medicine2014
miR-31 dysregulation in cystic fibrosis airways contributes to increased pulmonary cathepsin S production.
Article in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 85 citations in OpenAlex.
- Antiviral defenses are diminished at birth in cystic fibrosis pig airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Article
- The Histamine Four Receptor Regulates LFA-1 But Not Mac-1 -Dependent Neutrophil Adhesion and Inflammatory Functions.Inflammation · 2026Article
- Cathepsin S: a double-edged protease in barrier damage, neuroimmune inflammation, and tissue repair, with implications for dermatology.Frontiers in immunology · 2026Review
- Neutrophil-derived biomarkers in bronchiectasis: identifying a common therapeutic target.The European respiratory journal · 2025Review
- Dipeptidyl peptidase-1 inhibitors in bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Cathepsin S: molecular mechanisms in inflammatory and immunological processes.Frontiers in immunology · 2025Review
- CTSG is a prognostic marker involved in immune infiltration and inhibits tumor progression though the MAPK signaling pathway in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2024Article
- Inhibition of cathepsin L ameliorates inflammation through the A20/NF-κB pathway in endotoxin-induced acute lung injury.iScience · 2024Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Diminished airway host innate response in people with cystic fibrosis who experience frequent pulmonary exacerbations.The European respiratory journal · 2024Article
- Laboratory Tools to Predict CFTR Modulator Therapy Effectiveness and to Monitor Disease Severity in Cystic Fibrosis.Journal of personalized medicine · 2024Review
- Mycobacterium avium inhibits protein kinase C and MARCKS phosphorylation in human cystic fibrosis and non-cystic fibrosis cells.PloS one · 2024Article
- Mechanisms by which the cystic fibrosis transmembrane conductance regulator may influence SARS-CoV-2 infection and COVID-19 disease severity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Distinct mechanisms of dysfunctional antigen-presenting DCs and monocytes by single-cell sequencing in multiple myeloma.Cancer science · 2023Article
- Non-Coding RNAs in Pulmonary Diseases: Comparison of Different Airway-Derived Biosamples.International journal of molecular sciences · 2023Review
- Identification of Hub Genes in the Pathogenesis of Bronchiolitis Obliterans via Bioinformatic Analysis and Experimental Verification.Journal of inflammation research · 2023Article
- Piezo1 specific deletion in macrophage protects the progression of liver fibrosis in mice.Theranostics · 2023Article
- Cleavage of Occludin by Cigarette Smoke-Elicited Cathepsin S Increases Permeability of Lung Epithelial Cells.Antioxidants (Basel, Switzerland) · 2022Article
- DMBT1 is upregulated in cystic fibrosis, affects ciliary motility, and is reduced by acetylcysteine.Molecular and cellular pediatrics · 2022Article
- Noncoding RNAs as Promising Diagnostic Biomarkers and Therapeutic Targets in Intestinal Fibrosis of Crohn's Disease: The Path From Bench to Bedside.Inflammatory bowel diseases · 2021Review
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
rationaleCathepsin S (CTSS) activity is increased in bronchoalveolar lavage (BAL) fluid from patients with cystic fibrosis (CF). This activity contributes to lung inflammation via degradation of antimicrobial proteins, such as lactoferrin and members of the β-defensin family.
objectivesIn this study, we investigated the hypothesis that airway epithelial cells are a source of CTSS, and mechanisms underlying CTSS expression in the CF lung.
methodsProtease activity was determined using fluorogenic activity assays. Protein and mRNA expression were analyzed by ELISA, Western blotting, and reverse-transcriptase polymerase chain reaction. MEASUREMENTS AND MAIN
resultsIn contrast to neutrophil elastase, CTSS activity was detectable in 100% of CF BAL fluid samples from patients without Pseudomonas aeruginosa infection. In this study, we identified epithelial cells as a source of pulmonary CTSS activity with the demonstration that CF airway epithelial cells express and secrete significantly more CTSS than non-CF control cells in the absence of proinflammatory stimulation. Furthermore, levels of the transcription factor IRF-1 correlated with increased levels of its target gene CTSS. We discovered that miR-31, which is decreased in the CF airways, regulates IRF-1 in CF epithelial cells. Treating CF bronchial epithelial cells with a miR-31 mimic decreased IRF-1 protein levels with concomitant knockdown of CTSS expression and secretion.
conclusionsThe miR-31/IRF-1/CTSS pathway may play a functional role in the pathogenesis of CF lung disease and may open up new avenues for exploration in the search for an effective therapeutic target.
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