ArticlePLoS genetics2013
Positional cloning reveals strain-dependent expression of Trim16 to alter susceptibility to bleomycin-induced pulmonary fibrosis in mice.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Cordyceps cicadae polysaccharides attenuate diabetic nephropathy via the miR-30a-3p/TRIM16 axis.Journal of diabetes investigation · 2024Article
- Antifibrotic mechanism of avitinib in bleomycin-induced pulmonary fibrosis in mice.BMC pulmonary medicine · 2023Article
- Prognostic accuracy of a peripheral blood transcriptome signature in chronic hypersensitivity pneumonitis.Thorax · 2022Article
- Human antigen R promotes lung fibroblast differentiation to myofibroblasts and increases extracellular matrix production.Journal of cellular physiology · 2021Article
- Genes, other than Muc5b, play a role in bleomycin-induced lung fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Efficacy of bone marrow mesenchymal stem cell transplantation in animal models of pulmonary fibrosis after exposure to bleomycin: A meta-analysis.Experimental and therapeutic medicine · 2019Article
- Exploring Animal Models That Resemble Idiopathic Pulmonary Fibrosis.Frontiers in medicine · 2017Review
- TRIM16 suppresses the progression of prostate tumors by inhibiting the Snail signaling pathway.International journal of molecular medicine · 2016Article
- ER Adaptor SCAP Translocates and Recruits IRF3 to Perinuclear Microsome Induced by Cytosolic Microbial DNAs.PLoS pathogens · 2016Article
- TRIM16 inhibits proliferation and migration through regulation of interferon beta 1 in melanoma cells.Oncotarget · 2014Article
Corrections and comments
- Erratum issuedDepault, François [added]
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary fibrosis is a disease of significant morbidity, with no effective therapeutics and an as yet incompletely defined genetic basis. The chemotherapeutic agent bleomycin induces pulmonary fibrosis in susceptible C57BL/6J mice but not in mice of the C3H/HeJ strain, and this differential strain response has been used in prior studies to map bleomycin-induced pulmonary fibrosis susceptibility loci named Blmpf1 and Blmpf2. In this study we isolated the quantitative trait gene underlying Blmpf2 initially by histologically phenotyping the bleomycin-induced lung disease of sublines of congenic mice to reduce the linkage region to 13 genes. Of these genes, Trim16 was identified to have strain-dependent expression in the lung, which we determined was due to sequence variation in the promoter. Over-expression of Trim16 by plasmid injection increased pulmonary fibrosis, and bronchoalveolar lavage levels of both interleukin 12/23-p40 and neutrophils, in bleomycin treated B6.C3H-Blmpf2 subcongenic mice compared to subcongenic mice treated with bleomycin only, which follows the C57BL/6J versus C3H/HeJ strain difference in these traits. In summary we demonstrate that genetic variation in Trim16 leads to its strain-dependent expression, which alters susceptibility to bleomycin-induced pulmonary fibrosis in mice.
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