ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
MicroRNA-96 inhibits FoxO3a function in IPF fibroblasts on type I collagen matrix.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.
- Systematic review of overlapping microRNA patterns in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2023Pooled it
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Emerging delivery approaches for targeted pulmonary fibrosis treatment.Advanced drug delivery reviews · 2024Review
- Delivery of anti-microRNA-21 by lung-targeted liposomes for pulmonary fibrosis treatment.Molecular therapy. Nucleic acids · 2023Article
- Sirolimus-eluting airway stent reduces profibrotic Th17 cells and inhibits laryngotracheal stenosis.JCI insight · 2023Article
- FoxO3 and oxidative stress: a multifaceted role in cellular adaptation.Journal of molecular medicine (Berlin, Germany) · 2023Review
- More than a Genetic Code: Epigenetics of Lung Fibrosis.Molecular diagnosis & therapy · 2020Review
- Aberrant MicroRNAomics in Pulmonary Complications: Implications in Lung Health and Diseases.Molecular therapy. Nucleic acids · 2019Review
- Molecular determinants of mesenchymal cell activation in fibroproliferative diseases.Cellular and molecular life sciences : CMLS · 2019Review
- Fibroblasts from patients with idiopathic pulmonary fibrosis are resistant to cisplatin-induced cell death via enhanced CK2-dependent XRCC1 activity.Apoptosis : an international journal on programmed cell death · 2019Article
- P27 Promotes TGF-Canadian respiratory journal · 2019Article
- Molecular pathogenesis involved in human idiopathic pulmonary fibrosis based on an integrated microRNA‑mRNA interaction network.Molecular medicine reports · 2018Article
- Critical role of FOXO3a in carcinogenesis.Molecular cancer · 2018Review
- FoxM1-dependent RAD51 and BRCA2 signaling protects idiopathic pulmonary fibrosis fibroblasts from radiation-induced cell death.Cell death & disease · 2018Article
- The Role of the Mammalian Target of Rapamycin (mTOR) in Pulmonary Fibrosis.International journal of molecular sciences · 2018Review
- Article
- Treprostinil inhibits proliferation and extracellular matrix deposition by fibroblasts through cAMP activation.Scientific reports · 2018Article
- miR-96-5p prevents hepatic stellate cell activation by inhibiting autophagy via ATG7.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Posttranscriptional regulation of FOXO expression: microRNAs and beyond.British journal of pharmacology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a lethal and progressive lung disease characterized by persistent (myo)fibroblasts and the relentless accumulation of collagen matrix. Unlike normal lung fibroblasts, IPF lung fibroblasts have suppressed forkhead box O3a (FoxO3a) activity, which allows them to expand in this diseased environment. microRNA-96 (miR-96) has recently been found to directly bind to the 3'-untranslated region of FoxO3a mRNA, which subsequently inhibits its function. We examined whether aberrantly low FoxO3a expression is in part due to increased miR-96 levels in IPF fibroblasts on polymerized collagen, thereby causing IPF fibroblasts to maintain their pathological properties. miR-96 expression was upregulated in IPF fibroblasts compared with control fibroblasts when cultured on collagen. In contrast, FoxO3a mRNA levels were reduced in most IPF fibroblasts. However, when miR-96 function was inhibited, FoxO3a mRNA and protein expression were increased, suppressing IPF fibroblast proliferation and promoting their cell death in a dose-dependent fashion. Likewise, FoxO3a and its target proteins p21, p27, and Bim expression was also increased in the presence of a miR-96 inhibitor in IPF fibroblasts. However, when control fibroblasts were treated with miR-96 mimic, FoxO3a, p27, p21, and Bim mRNA and protein levels were decreased. In situ hybridization analysis further revealed the presence of enhanced miR-96 expression in cells within the fibroblastic foci of IPF lung tissue. Our results suggest that when IPF fibroblasts interact with collagen-rich matrix, pathologically altered miR-96 expression inhibits FoxO3a function, causing IPF fibroblasts to maintain their pathological phenotype, which may contribute to the progression of IPF.
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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.