ArticleToxicology research2017
MicroRNA-29b inhibits supernatants from silica-treated macrophages from inducing extracellular matrix synthesis in lung fibroblasts.
Article in Toxicology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Tissue-resident Klebsiella quasipneumoniae contributes to progression of idiopathic pulmonary fibrosis by triggering macrophages mitophagy in mice.Cell death discovery · 2025Article
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- MiR-148a-3p within HucMSC-Derived Extracellular Vesicles Suppresses Hsp90b1 to Prevent Fibroblast Collagen Synthesis and Secretion in Silica-Induced Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
- Cyanidin-3-galactoside fromFood science & nutrition · 2022Article
- Profiles of microRNA in aqueous humor of normal tension glaucoma patients using RNA sequencing.Scientific reports · 2021Article
- Crosstalk between MicroRNA and Oxidative Stress in Primary Open-Angle Glaucoma.International journal of molecular sciences · 2021Review
- Recent Research Progress (2015-2021) and Perspectives on the Pharmacological Effects and Mechanisms of Tanshinone IIA.Frontiers in pharmacology · 2021Review
- Harnessing noncoding RNA-based macrophage polarization: Emerging therapeutic opportunities for fibrosis.Immunity, inflammation and disease · 2020Review
- miR-29b attenuates histone deacetylase-4 mediated podocyte dysfunction and renal fibrosis in diabetic nephropathy.Journal of diabetes and metabolic disorders · 2020Article
- Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease.Frontiers in medicine · 2020Review
- Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiOJournal of toxicologic pathology · 2019Article
- MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.Molecular therapy. Nucleic acids · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM) components. The ECM is mainly secreted by myofibroblasts which are the activated state of fibroblasts. MicroRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified. In this study, we hypothesized that miR-29b might play a protective role in the progression of silicosis. MTT assay, qRT-PCR, immunofluorescence and western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Meanwhile they could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited ECM synthesis. These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.
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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.