ArticleScientific reports2015
p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- A small-molecule TNIK inhibitor targets fibrosis in preclinical and clinical models.Nature biotechnology · 2025Trial
- Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation.Respiratory research · 2024Article
- Exploring In Vivo Pulmonary and Splenic Toxicity Profiles of Silicon Quantum Dots in Mice.Materials (Basel, Switzerland) · 2024Article
- MicroRNA-495 suppresses pre-eclampsia via activation of p53/PUMA axis.Cell death discovery · 2022Article
- The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis.International journal of molecular sciences · 2021Review
- Underground Gold Miner Exposure to Noise, Diesel Particulate Matter and Crystalline Silica Dust.Journal of health & pollution · 2021Article
- Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.Cell & bioscience · 2021Article
- Investigation of MicroRNA and transcription factor mediated regulatory network for silicosis using systems biology approach.Scientific reports · 2021Article
- Role of PUMA in the methamphetamine-induced migration of microglia.Metabolic brain disease · 2019Article
- CircHECTD1 mediates pulmonary fibroblast activationTherapeutic advances in chronic disease · 2019Article
- circHECTD1 promotes the silica-induced pulmonary endothelial-mesenchymal transition via HECTD1.Cell death & disease · 2018Article
- Silica exposure increases the risk of stroke but not myocardial infarction-A retrospective cohort study.PloS one · 2018Article
- circRNA Mediates Silica-Induced Macrophage Activation Via HECTD1/ZC3H12A-Dependent Ubiquitination.Theranostics · 2018Article
- circHIPK2-mediated σ-1R promotes endoplasmic reticulum stress in human pulmonary fibroblasts exposed to silica.Cell death & disease · 2017Article
- Radiation induced pulmonary fibrosis as a model of progressive fibrosis: Contributions of DNA damage, inflammatory response and cellular senescence genes.Experimental lung research · 2017Article
- BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis.Cell death & disease · 2017Article
- Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy.Particle and fibre toxicology · 2016Article
- MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Interplay between Cellular and Molecular Inflammatory Mediators in Lung Cancer.Mediators of inflammation · 2016Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phagocytosis of SiO2 into the lung causes an inflammatory cascade that results in fibroblast proliferation and migration, followed by fibrosis. Clinical evidence has indicated that the activation of alveolar macrophages by SiO2 produces rapid and sustained inflammation characterized by the generation of monocyte chemotactic protein 1, which, in turn, induces fibrosis. However, the details of events downstream of monocyte chemotactic protein 1 activity in pulmonary fibroblasts remain unclear. Here, to elucidate the role of p53 in fibrosis induced by silica, both the upstream molecular mechanisms and the functional effects on cell proliferation and migration were investigated. Experiments using primary cultured adult human pulmonary fibroblasts led to the following results: 1) SiO2 treatment resulted in a rapid and sustained increase in p53 and PUMA protein levels; 2) the MAPK and PI3K pathways were involved in the SiO2-induced alteration of p53 and PUMA expression; and 3) RNA interference targeting p53 and PUMA prevented the SiO2-induced increases in fibroblast activation and migration. Our study elucidated a link between SiO2-induced p53/PUMA expression in fibroblasts and cell migration, thereby providing novel insight into the potential use of p53/PUMA in the development of novel therapeutic strategies for silicosis 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.