ArticleThe American journal of pathology1999
Reduced tumor necrosis factor-alpha and transforming growth factor-beta1 expression in the lungs of inbred mice that fail to develop fibroproliferative lesions consequent to asbestos exposure.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 67 citations in OpenAlex.
- The protective effects of ambroxol on radiation lung injury and influence on production of transforming growth factor beta1 and tumor necrosis factor alpha.Medical oncology (Northwood, London, England) · 2010Trial
- Targeting the NLRP3 inflammasome and associated cytokines in scleroderma associated interstitial lung disease.Frontiers in cell and developmental biology · 2023Review
- Modifiers of TGF-β1 effector function as novel therapeutic targets of pulmonary fibrosis.The Korean journal of internal medicine · 2014Review
- Effects of lipopolysaccharide on the response of C57BL/6J mice to whole thorax irradiation.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2012Article
- Allele-specific effects of ecSOD on asbestos-induced fibroproliferative lung disease in mice.Free radical biology & medicine · 2011Article
- Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos.Journal of toxicology and environmental health. Part B, Critical reviews · 2011Review
- TNF-alpha induces TGF-beta1 expression in lung fibroblasts at the transcriptional level via AP-1 activation.Journal of cellular and molecular medicine · 2009Article
- Laser capture microdissection reveals dose-response of gene expression in situ consequent to asbestos exposure.International journal of experimental pathology · 2007Article
- Titration of non-replicating adenovirus as a vector for transducing active TGF-beta1 gene expression causing inflammation and fibrogenesis in the lungs of C57BL/6 mice.International journal of experimental pathology · 2002Article
- Interstitial fibrosis and growth factors.Environmental health perspectives · 2000Review
- Increased phosphorylated extracellular signal-regulated kinase immunoreactivity associated with proliferative and morphologic lung alterations after chrysotile asbestos inhalation in mice.The American journal of pathology · 2000Article
- Emphysematous lesions, inflammation, and fibrosis in the lungs of transgenic mice overexpressing platelet-derived growth factor.The American journal of pathology · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta mRNA and protein expression and the degree of fibroproliferative response to inhaled asbestos fibers are clearly reduced in the 129 inbred mouse strain as compared with typical fibrogenesis observed in the C57BL/6 inbred strain. The C57BL/6 mice showed prominent lesions at bronchiolar-alveolar duct (BAD) junctions where asbestos fibers deposit and responding macrophages accumulate. The 129 mice, however, were generally indistinguishable from controls even though the numbers of asbestos fibers deposited in the lungs of all exposed animals were the same. Quantitative morphometry of H&E-stained lung sections comparing the C57BL/6 and 129 mice showed significantly less mean cross-sectional area of the BAD junctions in the 129 animals, apparent at both 48 hours and 4 weeks after exposure. In addition, fewer macrophages had accumulated at these sites in the 129 mice. Nuclear bromodeoxyuridine immunostaining demonstrated that the number of proliferating cells at first alveolar duct bifurcations and in adjacent terminal bronchioles was significantly reduced in the 129 strain compared with C57BL/6 mice at 48 hours after exposure (P < 0.01). TNF-alpha and TGF-beta1 gene expression, as measured by in situ hybridization, was reduced in the 129 mice at 48 hours after exposure, and expression of TNF-alpha and TGF-beta1 protein, as measured by immunohistochemistry, was similarly reduced or absent in the 129 animals. We postulate that the protection afforded the 129 mice is related to reduction of growth factor expression by the bronchiolar-alveolar epithelium and lung macrophages.
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Registered trials
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