ArticleFibrogenesis & tissue repair2011
Local apoptosis promotes collagen production by monocyte-derived cells in transforming growth factor β1-induced lung fibrosis.
Article in Fibrogenesis & tissue repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
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- Review: interstitial lung disease associated with systemic sclerosis and idiopathic pulmonary fibrosis: how similar and distinct?Arthritis & rheumatology (Hoboken, N.J.) · 2014Review
- Chitinase 3-like 1 suppresses injury and promotes fibroproliferative responses in Mammalian lung fibrosis.Science translational medicine · 2014Article
- Functional effects of TGF-β1 on mesenchymal stem cell mobilization in cockroach allergen-induced asthma.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Association of Interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Future directions in idiopathic pulmonary fibrosis research. An NHLBI workshop report.American journal of respiratory and critical care medicine · 2014Article
- Rapid granulation tissue regeneration by intracellular ATP delivery--a comparison with Regranex.PloS one · 2014Article
- ADAM metallopeptidase domain 33 (ADAM33): a promising target for asthma.Mediators of inflammation · 2014Review
- Prostatic inflammation induces fibrosis in a mouse model of chronic bacterial infection.PloS one · 2014Article
- Aryl hydrocarbon receptor (AhR) modulates cockroach allergen-induced immune responses through active TGFβ1 release.Mediators of inflammation · 2014Article
- Regulation and Relevance of Myofibroblast Responses in Idiopathic Pulmonary Fibrosis.Current pathobiology reports · 2013Article
- Efferocytosis and lung disease.Chest · 2013Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCollagen-containing leukocytes (CD45+Col-I+) accumulate in diseased and fibrotic tissues. However, the precise identity of these cells and whether injury is required for their recruitment remain unknown. Using a murine model of pulmonary fibrosis in which an inducible, bioactive form of the human transforming growth factor (TGF)-β1 gene is targeted to the lung, we characterized the cell surface phenotype of collagen-containing CD45+ cells in the lung and tested the hypothesis that apoptotic cell death responses are essential to the accumulation of CD45+Col-I+ cells.
resultsOur studies demonstrate that CD45+Col-I+ cells appearing in the TGF-β1-exposed murine lung express markers of the monocyte lineage. Inhibition of apoptosis via pharmacological caspase blockade led to a significant reduction in CD45+Col-I+ cells, which appear to accumulate independently of alternatively activated macrophages. There are also increased levels of apoptosis and greater numbers of CD45+Col-I+ in the lung tissue of patients with two distinct forms of fibrotic lung disease, idiopathic pulmonary fibrosis and connective tissue disease-related interstitial lung disease, when compared to lung from healthy normal controls. These findings are accompanied by an increase in collagen production in cultured monocytes obtained from subjects with fibrotic lung disease. Treatment of these cultured cells with the caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD/fmk) reduces both apoptosis and collagen production in all subjects.
conclusionsInterventions that prevent collagen production by monocytes via modulation of caspase activation and of apoptosis may be ameliorative in monocyte-associated, TGF-β1-driven processes such as pulmonary fibrosis.
Identifiers
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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.