ArticleThe American journal of pathology2009
Matrilysin (Matrix Metalloproteinase-7) regulates anti-inflammatory and antifibrotic pulmonary dendritic cells that express CD103 (alpha(E)beta(7)-integrin).
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Shared and unique transcriptomic signature genes and pathways among biopsy, peripheral blood mononuclear cells and bronchoalveolar lavage samples in IPF patients revealed using comparative meta-transcriptome analysis.Tuberkuloz ve toraks · 2024Pooled it
- Matrix metalloproteinases and tissue damage in HIV-tuberculosis immune reconstitution inflammatory syndrome.European journal of immunology · 2014Trial
- Evidence that metformin promotes fibrosis resolutionActa pharmaceutica Sinica. B · 2025Article
- Proteins associated with preserved ratio impaired spirometry.ERJ open research · 2025Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Matrix metalloproteinase-7 is dispensable in a mouse model of sepsis-induced acute lung injury.PloS one · 2025Article
- Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024Review
- Molecular insights using spatial transcriptomics of the distal lung in congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Amelioration of Pulmonary Fibrosis by Matrix Metalloproteinase-2 Overexpression.International journal of molecular sciences · 2023Article
- Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play.International journal of molecular sciences · 2022Review
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Distinct Metalloproteinase Expression and Functions in Systemic Sclerosis and Fibrosis: What We Know and the Potential for Intervention.Frontiers in physiology · 2021Review
- Attenuation of pulmonary injury by an inhaled MMP inhibitor in the endotoxin lung injury model.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury.Malaria journal · 2020Article
- Alveolar heparan sulfate shedding impedes recovery from bleomycin-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- A Tale of Two Proteolytic Machines: Matrix Metalloproteinases and the Ubiquitin-Proteasome System in Pulmonary Fibrosis.International journal of molecular sciences · 2020Review
- Human fibroblast-macrophage tissue spheroids demonstrate ratio-dependent fibrotic activity for in vitro fibrogenesis model development.Biomaterials science · 2020Article
- Circulating matrix metalloproteinases and tissue metalloproteinase inhibitors in patients with idiopathic pulmonary fibrosis in the multicenter IPF-PRO Registry cohort.BMC pulmonary medicine · 2020Observational
- Matrix metalloproteinases in emphysema.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Association of the MMP7 -181A>G Promoter Polymorphism with Early Onset of Chronic Obstructive Pulmonary Disease.Balkan journal of medical genetics : BJMG · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
The E-cadherin receptor CD103 (alpha(E)beta(7)-integrin) is expressed on specific populations of pulmonary dendritic cells (DC) and T cells. However, CD103 function in the lung is not well understood. Matrilysin (MMP-7) expression is increased in lung injury and cleaves E-cadherin from injured lung epithelium. Thus, to assess matrilysin effects on CD103-E-cadherin interactions in lung injury, wild-type, CD103(-/-), and Mmp7(-/-) mice, in which E-cadherin isn't cleaved in the lung, were treated with bleomycin or bleomycin with nFMLP to reverse the defect in acute neutrophil influx seen in Mmp7(-/-) mice. Pulmonary CD103(+) DC were significantly increased in injured wild-type compared with Mmp7(-/-) mice, and CD103(+) leukocytes showed significantly enhanced interaction with E-cadherin on injured wild-type epithelium than with Mmp7(-/-) epithelium in vitro and in vivo. Bleomycin-treated CD103(-/-) mice had persistent neutrophilic inflammation, increased fibrosis, and increased mortality compared with wild-type mice, a phenotype that was partially recapitulated in bleomycin/nFMLP-treated Mmp7(-/-) mice. Soluble E-cadherin increased IL-12 and IL-10 and reduced IL-6 mRNA expression in wild-type bone marrow-derived DC but not in CD103(-/-) bone marrow-derived DC. Similar mRNA patterns were seen in lungs of bleomycin-injured wild-type, but not CD103(-/-) or Mmp7(-/-), mice. In conclusion, matrilysin regulates pulmonary localization of DC that express CD103, and E-cadherin cleavage may activate CD103(+) DC to limit inflammation and inhibit fibrosis.
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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.