ArticleInternational journal of experimental pathology2002
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.
Article in International journal of experimental pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- TGF-β induces excessive pulmonary IL-6 secretion in cystic fibrosis via PI3K.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Hypoxia Induces Alterations in the Circadian Rhythm in Patients with Chronic Respiratory Diseases.Cells · 2023Review
- CFTR dysfunction in smooth muscle drives TGFβ dependent airway hyperreactivity.Respiratory research · 2023Article
- Is there a role for specialized pro-resolving mediators in pulmonary fibrosis?Pharmacology & therapeutics · 2023Review
- Repetitive schistosoma exposure causes perivascular lung fibrosis and persistent pulmonary hypertension.Clinical science (London, England : 1979) · 2023Article
- MMP-1 and ADAM10 as Targets for Therapeutic Intervention in Idiopathic Pulmonary Fibrosis.ACS pharmacology & translational science · 2022Article
- Article
- Subacute TGFβ Exposure Drives Airway Hyperresponsiveness in Cystic Fibrosis Mice through the PI3K Pathway.American journal of respiratory cell and molecular biology · 2020Article
- Subacute TGFβ expression drives inflammation, goblet cell hyperplasia, and pulmonary function abnormalities in mice with effects dependent on CFTR function.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- BRD4 mediates NF-κB-dependent epithelial-mesenchymal transition and pulmonary fibrosis via transcriptional elongation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Regulation of transforming growth factor-beta1 (TGF-β1)-induced pro-fibrotic activities by circadian clock gene BMAL1.Respiratory research · 2016Article
- Thiol-redox antioxidants protect against lung vascular endothelial cytoskeletal alterations caused by pulmonary fibrosis inducer, bleomycin: comparison between classical thiol-protectant, N-acetyl-L-cysteine, and novel thiol antioxidant, N,N'-bis-2-mercaptoethyl isophthalamide.Toxicology mechanisms and methods · 2012Article
- TGFβ signaling in lung epithelium regulates bleomycin-induced alveolar injury and fibroblast recruitment.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Interstitial lung diseases in children.Orphanet journal of rare diseases · 2010Review
- TGF-β: Titan of Lung Fibrogenesis.Current enzyme inhibition · 2010Article
- Transforming growth factor-beta1 induces heparan sulfate 6-O-endosulfatase 1 expression in vitro and in vivo.The Journal of biological chemistry · 2008Article
- Progressive pulmonary fibrosis is mediated by TGF-beta isoform 1 but not TGF-beta3.The international journal of biochemistry & cell biology · 2008Article
- Laser capture microdissection reveals dose-response of gene expression in situ consequent to asbestos exposure.International journal of experimental pathology · 2007Article
- Early growth response gene 1-mediated apoptosis is essential for transforming growth factor beta1-induced pulmonary fibrosis.The Journal of experimental medicine · 2004Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Investigators have shown that interstitial pulmonary fibrosis (IPF) can be induced in rats by overexpressing transforming growth factor beta1 (TGF-beta1) through a replication-deficient recombinant adenovirus vector instilled into the lungs (Sime et al. 1997). We have shown that this vector induces IPF in fibrogenic-resistant tumour necrosis factor alpha-receptor knockout (TNF-alphaRKO) mice (Liu et al. 2001). The object of our studies is to understand how peptide growth factors, such as TGF-beta1, mediate interstitial lung disease (ILD). To do so, we must be able to manipulate the dose of the factor and sort out its effects on multiple other mediators in the lung parenchyma. As a step in this complex process, in the studies reported here, we have determined the concentrations of the recombinant adenovirus vector carrying the gene for porcine active TGF-beta1 (AVTGFbeta1) that have little apparent effect, cause clear induction of disease, or severe disease. The disease largely resolves by 28 days in all cases, thus providing a valuable model to understand the mechanisms of the IPF that is mediated, at least in part, by TGF-beta1. The findings here show that 10(6) plaque-forming units (pfu) of AVTGFbeta1, provide essentially a 'no-effect' dose, but even this amount of TGF-beta1 causes a significant increase in whole-lung collagen by day 28 after treatment. In contrast, 10(8) and 10(9) pfu cause severe IPF in 4 days, whereas 10(7) and 5 x 10(7) are intermediate for all parameters studied, i.e. TGF-beta protein, inflammatory cells, cell proliferation, pro-alpha 1(I) collagen gene expression and whole-lung collagen accumulation, and expression of growth factors such as TGF-beta1, TNF-alpha and PDGF-A and -B. Interestingly enough, TGF-beta1, as a potent blocker of epithelial cell proliferation, appears to suppress airway epithelial cell growth that would be expected during the inflammatory phase of IPF. Thus, this model system helps us to understand some quantitative aspects of TGF-beta1 biological activity and allows us to manipulate this potent factor as a mediator of interstitial fibrogenesis.
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