ArticleInternational journal of molecular sciences2018
miR-542-5p Attenuates Fibroblast Activation by Targeting Integrin α6 in Silica-Induced Pulmonary Fibrosis.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- The emerging roles of microRNAs in pneumoconiosis: pathogenic mechanisms and clinical implications.Frontiers in cell and developmental biology · 2026Review
- Multi-omics approaches in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic targets and precision medicine.Frontiers in pharmacology · 2026Review
- Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.Nature communications · 2025Article
- Integrins and pulmonary fibrosis: Pathogenic roles and therapeutic opportunities.Biomolecules & biomedicine · 2025Review
- The role of epigenetics in pulmonary fibrosis: recent advances in mechanistic insights and therapeutic implications.Frontiers in molecular biosciences · 2025Review
- Si-ITGA6-Loaded Liposomes Inhibit Capsule Fibrosis via the FAK/PI3K/Akt Signaling Pathway in Adhesive Capsulitis of Shoulder.International journal of nanomedicine · 2025Article
- Hsa_circ_0004214 involved in the epithelial-mesenchymal transition induced by beryllium sulfate through modulating JAK-STAT signaling pathway.Toxicology research · 2024Article
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- microRNA-141-3p mediates epithelial cell proliferation, apoptosis, and epithelial-mesenchymal transition and alleviates pulmonary fibrosis in mice via Spred2.Histology and histopathology · 2023Article
- Enhancement of Zyxin Promotes Skin Fibrosis by Regulating FAK/PI3K/AKT and TGF-β Signaling Pathways via Integrins.International journal of biological sciences · 2023Article
- The emerging role of epigenetic regulation in the progression of silicosis.Clinical epigenetics · 2022Review
- The Genetic and Epigenetic Footprint in Idiopathic Pulmonary Fibrosis and Familial Pulmonary Fibrosis: A State-of-the-Art Review.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- Integrin α6 overexpression promotes lymphangiogenesis and lymphatic metastasis via activating the NF-κB signaling pathway in lung adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- The circ-PITX1 promotes non-small cell lung cancer development via the miR-30e-5p/ITGA6 axis.Cell cycle (Georgetown, Tex.) · 2022Article
- Blocking ATM Attenuates SKOV3 Cell Proliferation and Migration by DisturbingFrontiers in oncology · 2022Article
- IntegrinJournal of oncology · 2022Article
- Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022Review
- Cedrol alleviates the apoptosis and inflammatory response of IL-1β-treated chondrocytes by promoting miR-542-5p expression.In vitro cellular & developmental biology. Animal · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Silicosis is a very serious occupational disease and it features pathological manifestations of inflammatory infiltration, excessive proliferation of fibroblasts and massive depositions of the extracellular matrix in the lungs. Recent studies described the roles of a variety of microRNAs (miRNAs) in fibrotic diseases. Here, we aimed to explore the potential mechanism of miR-542-5p in the activation of lung fibroblasts. To induce a pulmonary fibrosis mouse model, silica suspension and the miR-542-5p agomir were administered to mice by intratracheal instillation and tail vein injection. We found that miR-542-5p was significantly decreased in mouse fibrotic lung tissues and up-regulation of miR-542-5p visually attenuated a series of fibrotic lesions, including alveolar structural damage, alveolar interstitial thickening and silica-induced nodule formation. The down-regulation of miR-542-5p was also observed in mouse fibroblast (NIH-3T3) treated with transforming growth factor β1 (TGF-β1). The proliferation and migration ability of NIH-3T3 cells were also inhibited by the transfection of miR-542-5p mimic. Integrin α6 (Itga6), reported as a cell surface protein associated with fibroblast proliferation, was confirmed to be a direct target of miR-542-5p. The knockdown of Itga6 significantly inhibited the phosphorylation of FAK/PI3K/AKT. In conclusion, miR-542-5p has a potential function for reducing the proliferation of fibroblasts and inhibiting silica-induced pulmonary fibrosis, which might be partially realized by directly binding to Itga6. Our data suggested that miR-542-5p might be a new therapeutic target for silicosis or other pulmonary fibrosis.
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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.