ArticleAmerican journal of respiratory and critical care medicine2018
MicroRNA-145 Antagonism Reverses TGF-β Inhibition of F508del CFTR Correction in Airway Epithelia.
Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 63 citations in OpenAlex.
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- Antifibrotic Drugs Regulate the Expression of Epithelial Sodium Channels in the Lungs.Advances in respiratory medicine · 2026Article
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
- Peptide Nucleic Acids for MicroRNAs Targeting: Updates and Future Perspectives.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Identification of Proteins and MicroRNAs with Prognostic Value for Assisted Reproduction Technology Outcomes in Follicular Fluid of Women with Endometriosis: A Pilot Study.International journal of molecular sciences · 2025Article
- Diagnosis and Emerging Biomarkers of Cystic Fibrosis-Related Kidney Disease (CFKD).Journal of clinical medicine · 2025Review
- Therapeutic strategies to reverse cigarette smoke-induced ion channel and mucociliary dysfunction in COPD airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Perspectives in MicroRNA Therapeutics for Cystic Fibrosis.Non-coding RNA · 2025Review
- Cystic fibrosis.Nature reviews. Disease primers · 2024Review
- Disrupting the TGF-β-Wnt Balance to Control the Polarity of the Cystic Fibrosis Airway Epithelium.American journal of respiratory cell and molecular biology · 2024Article
- Laboratory Tools to Predict CFTR Modulator Therapy Effectiveness and to Monitor Disease Severity in Cystic Fibrosis.Journal of personalized medicine · 2024Review
- 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
- Furin as a therapeutic target in cystic fibrosis airways disease.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Article
- Cystic fibrosis transmembrane conductance regulator in COPD: a role in respiratory epithelium and beyond.The European respiratory journal · 2023Review
- Non-Coding RNAs in Pulmonary Diseases: Comparison of Different Airway-Derived Biosamples.International journal of molecular sciences · 2023Review
- The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function.International journal of molecular sciences · 2022Article
- Exploring YAP1-centered networks linking dysfunctional CFTR to epithelial-mesenchymal transition.Life science alliance · 2022Article
- Combined Treatment of Bronchial Epithelial Calu-3 Cells with Peptide Nucleic Acids Targeting miR-145-5p and miR-101-3p: Synergistic Enhancement of the Expression of the Cystic Fibrosis Transmembrane Conductance Regulator (International journal of molecular sciences · 2022Article
- SARS-CoV-2 nucleocapsid protein triggers hyperinflammation via protein-protein interaction-mediated intracellular ClSignal transduction and targeted therapy · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleMicroRNAs (miRNAs) destabilize mRNA transcripts and inhibit protein translation. miR-145 is of particular interest in cystic fibrosis (CF) as it has a direct binding site in the 3'-untranslated region of CFTR (cystic fibrosis transmembrane conductance regulator) and is upregulated by the CF genetic modifier TGF (transforming growth factor)-β.
objectivesTo demonstrate that miR-145 mediates TGF-β inhibition of CFTR synthesis and function in airway epithelia.
methodsPrimary human CF (F508del homozygous) and non-CF airway epithelial cells were grown to terminal differentiation at the air-liquid interface on permeable supports. TGF-β (5 ng/ml), a miR-145 mimic (20 nM), and a miR-145 antagonist (20 nM) were used to manipulate CFTR function. In CF cells, lumacaftor (3 μM) and ivacaftor (10 μM) corrected mutant F508del CFTR. Quantification of CFTR mRNA, protein, and function was done by standard techniques. MEASUREMENTS AND MAIN
resultsmiR-145 is increased fourfold in CF BAL fluid compared with non-CF (P < 0.01) and increased 10-fold in CF primary airway epithelial cells (P < 0.01). Exogenous TGF-β doubles miR-145 expression (P < 0.05), halves wild-type CFTR mRNA and protein levels (P < 0.01), and nullifies lumacaftor/ivacaftor F508del CFTR correction. miR-145 overexpression similarly decreases wild-type CFTR protein synthesis (P < 0.01) and function (P < 0.05), and eliminates F508del corrector benefit. miR-145 antagonism blocks TGF-β suppression of CFTR and enhances lumacaftor correction of F508del CFTR.
conclusionsmiR-145 mediates TGF-β inhibition of CFTR synthesis and function in airway epithelia. Specific antagonists to miR-145 interrupt TGF-β signaling to restore F508del CFTR modulation. miR-145 antagonism may offer a novel therapeutic opportunity to enhance therapeutic benefit of F508del CFTR correction in CF epithelia.
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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.