ArticleThe American journal of pathology2008
Tissue inhibitor of metalloproteinase-1 moderates airway re-epithelialization by regulating matrilysin activity.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Functional and molecular insights in topical wound healing by ascorbic acid.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Modulation of the Epithelial-mesenchymal transition process by Forkhead Box C2 in the repair of airway epithelium after injury.Respiratory research · 2025Article
- Matrix metalloproteinases and tissue inhibitors in multiple myeloma: promote or inhibit?Frontiers in oncology · 2023Review
- Role of matrix metalloproteinase in wound healing.American journal of translational research · 2022Review
- Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles.JCI insight · 2019Article
- Characterization of the early molecular changes in the glomeruli of Cd151Scientific reports · 2017Article
- Defensins Potentiate a Neutralizing Antibody Response to Enteric Viral Infection.PLoS pathogens · 2016Article
- Transcriptome profiling reveals distinctive traits of retinol metabolism and neonatal parallels in the MRL/MpJ mouse.BMC genomics · 2015Article
- Angiotensin receptors as sensitive markers of acute bronchiole injury after lung transplantation.Lung · 2014Article
- Diverse functions of matrix metalloproteinases during fibrosis.Disease models & mechanisms · 2014Review
- Matrix metalloproteinase-7 coordinates airway epithelial injury response and differentiation of ciliated cells.American journal of respiratory cell and molecular biology · 2013Article
- Matrilysin (MMP-7) inhibition of BMP-7 induced renal tubular branching morphogenesis suggests a role in the pathogenesis of human renal dysplasia.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- Epilysin (matrix metalloproteinase-28) contributes to airway epithelial cell survival.Respiratory research · 2011Article
- Obliterative airway remodeling: molecular evidence for shared pathways in transplanted and native lungs.The American journal of pathology · 2011Article
- The loss of tuberin promotes cell invasion through the ß-catenin pathway.American journal of respiratory cell and molecular biology · 2010Article
- Mycobacterium bovis-BCG vaccination induces specific pulmonary transcriptome biosignatures in mice.PloS one · 2010Article
- Epithelial repair mechanisms in the lung.American journal of physiology. Lung cellular and molecular physiology · 2010Review
- Modulation of ozone-sensitive genes in alpha-tocopherol transfer protein null mice.Inhalation toxicology · 2010Article
- Tissue inhibitor of metalloproteinases 3 regulates resolution of inflammation following acute lung injury.The American journal of pathology · 2010Article
- Role of matrix metalloproteinases in epithelial migration.Journal of cellular biochemistry · 2009Review
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11 authors.
Funding
Abstract
Obliterative bronchiolitis (OB) is the histopathological finding in chronic lung allograft rejection. Mounting evidence suggests that epithelial damage drives the development of airway fibrosis in OB. Tissue inhibitor of metalloproteinase (TIMP)-1 expression increases in lung allografts and is associated with the onset of allograft rejection. Furthermore, in a mouse model of OB, airway obliteration is reduced in TIMP-1-deficient mice. Matrilysin (matrix metallproteinase-7) is essential for airway epithelial repair and is required for the re-epithelialization of airway wounds by facilitating cell migration; therefore, the goal of this study was to determine whether TIMP-1 inhibits re-epithelialization through matrilysin. We found that TIMP-1 and matrilysin co-localized in the epithelium of human lungs with OB and both co-localized and co-immunoprecipitated in wounded primary airway epithelial cultures. TIMP-1-deficient cultures migrated faster, and epithelial cells spread to a greater extent compared with wild-type cultures. TIMP-1 also inhibited matrilysin-mediated cell migration and spreading in vitro. In vivo, TIMP-1 deficiency enhanced airway re-epithelialization after naphthalene injury. Furthermore, TIMP-1 and matrilysin co-localized in airway epithelial cells adjacent to the wound edge. Our data demonstrate that TIMP-1 interacts with matrix metalloproteinases and regulates matrilysin activity during airway epithelial repair. Furthermore, we speculate that TIMP-1 overexpression restricts airway re-epithelialization by inhibiting matrilysin activity, contributing to a stereotypic injury response that promotes airway fibrosis via bronchiole airway epithelial damage and obliteration.
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