ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Matrix metalloproteinase (MMP)-19-deficient fibroblasts display a profibrotic phenotype.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 63 citations in OpenAlex.
- TRPML1 suppresses pulmonary fibrosis by limiting collagen and elastin deposition.The EMBO journal · 2026Article
- Mas1 Receptor Activation is Necessary and Sufficient to Transduce ACE2 Effect in PAH, But Ang(1-7) Alone is Insufficient.Pulmonary circulation · 2025Article
- Observational
- An integrated cell atlas of the lung in health and disease.Nature medicine · 2023Article
- Amelioration of Pulmonary Fibrosis by Matrix Metalloproteinase-2 Overexpression.International journal of molecular sciences · 2023Article
- Farnesyl diphosphate synthase promotes cell proliferation by regulating gene expression and alternative splicing profiles in HeLa cells.Oncology letters · 2023Article
- Endothelial cell-derived MMP19 promotes pulmonary fibrosis by inducing E(nd)MT and monocyte infiltration.Cell communication and signaling : CCS · 2023Article
- The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023Review
- Identification of immune biomarkers associated with basement membranes in idiopathic pulmonary fibrosis and their pan-cancer analysis.Frontiers in genetics · 2023Article
- Construction of the axolotl cell landscape using combinatorial hybridization sequencing at single-cell resolution.Nature communications · 2022Article
- Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play.International journal of molecular sciences · 2022Review
- Distinct Adipogenic and Fibrogenic Differentiation Capacities of Mesenchymal Stromal Cells from Pancreas and White Adipose Tissue.International journal of molecular sciences · 2022Article
- Atorvastatin and ezetimibe protect against hypercholesterolemia-induced lung oxidative stress, inflammation, and fibrosis in rats.Frontiers in medicine · 2022Article
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Autophagy in chronic lung disease.Progress in molecular biology and translational science · 2020Review
- Quercetin is able to alleviate TGF-β-induced fibrosis in renal tubular epithelial cells by suppressing miR-21.Experimental and therapeutic medicine · 2018Article
- A positive feedback loop bi-stably activates fibroblasts.Nature communications · 2018Article
- The Ewing Sarcoma Secretome and Its Response to Activation of Wnt/beta-catenin Signaling.Molecular & cellular proteomics : MCP · 2018Article
- MicroRNA-21 in Skin Fibrosis: Potential for Diagnosis and Treatment.Molecular diagnosis & therapy · 2017Review
- Photobiomodulation therapy improves both inflammatory and fibrotic parameters in experimental model of lung fibrosis in mice.Lasers in medical science · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and usually lethal interstitial lung disease of unknown etiology characterized by aberrant activation of epithelial cells that induce the migration, proliferation and activation of fibroblasts. The resulting distinctive fibroblastic/myofibroblastic foci are responsible for the excessive extracellular matrix (ECM) production and abnormal lung remodeling. We have recently found that matrix metalloproteinase 19 (MMP-19)-deficient (Mmp19-/-) mice develop an exaggerated bleomycin-induced lung fibrosis, but the mechanisms are unclear. In this study, we explored the effect of MMP-19 deficiency on fibroblast gene expression and cell behavior. Microarray analysis of Mmp19-/- lung fibroblasts revealed the dysregulation of several profibrotic pathways, including ECM formation, migration, proliferation, and autophagy. Functional studies confirmed these findings. Compared with wild-type mice, Mmp19-/- lung fibroblasts showed increased α1 (I) collagen gene and collagen protein production at baseline and after transforming growth factor-β treatment and increased smooth muscle-α actin expression (P < 0.05). Likewise, Mmp19-deficient lung fibroblasts showed a significant increase in proliferation (P < 0.01) and in transmigration and locomotion over Boyden chambers coated with type I collagen or with Matrigel (P < 0.05). These findings suggest that, in lung fibroblasts, MMP-19 has strong regulatory effects on the synthesis of key ECM components, on fibroblast to myofibroblast differentiation, and in migration and proliferation.
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Registered trials
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