ArticleThe Journal of biological chemistry2015
Recruitment of Matrix Metalloproteinase-9 (MMP-9) to the Fibroblast Cell Surface by Lysyl Hydroxylase 3 (LH3) Triggers Transforming Growth Factor-β (TGF-β) Activation and Fibroblast Differentiation.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 87 citations in OpenAlex.
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- Multi-Omics Insights into Chronic Rhinosinusitis with Nasal Polyps: A Review of Lipidomics, Proteomics, and Transcriptomics.Journal of inflammation research · 2026Review
- Heterologous expression and functional characterization of recombinant arenin to assess its anticancer and wound-healing potential.Bioresources and bioprocessing · 2025Article
- Mesenchymal stem cell-derived exosomes: a new hope for improving asthma airway remodeling.Annals of medicine · 2025Review
- BDNF-driven synaptic plasticity requires autocrine matrix metalloproteinase-9 activity.Science advances · 2025Article
- An orally bioavailable BRD4 inhibitor disrupts expansion of a pathogenic epithelial-mesenchymal niche in bleomycin-induced fibrosis.Respiratory research · 2025Article
- Matrix Metalloproteinase-9: A Key Diagnostic Biomarker in Cancer Progression.Current drug targets · 2025Review
- Cancer-associated fibroblasts: heterogeneity, tumorigenicity and therapeutic targets.Molecular biomedicine · 2024Review
- The dysadherin/MMP9 axis modifies the extracellular matrix to accelerate colorectal cancer progression.Nature communications · 2024Article
- Extracellular glucose triggers metabolic reprogramming of cultured human bronchial epithelial cells and indirect fibroblast activation.FEBS open bio · 2024Article
- Proteolytic Vesicles Derived fromBiomedicines · 2024Article
- The BAP31/miR-181a-5p/RECK axis promotes angiogenesis in colorectal cancerFrontiers in oncology · 2023Article
- Innate Immunity, Epithelial Plasticity, and Remodeling in Asthma.Advances in experimental medicine and biology · 2023Article
- Ivermectin Affects Neutrophil-Induced Inflammation through Inhibition of Hydroxylysine but Stimulation of Cathepsin G and Phenylalanine Secretion.Biomedicines · 2022Article
- Transforming Growth Factor-β Receptor-Mediated, p38 Mitogen-Activated Protein Kinase-Dependent Signaling Drives Enhanced Myofibroblast Differentiation during Skin Wound Healing in Mice Lacking Hyaluronan Synthases 1 and 3.The American journal of pathology · 2022Article
- CD147 contributes to SARS-CoV-2-induced pulmonary fibrosis.Signal transduction and targeted therapy · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solid tumor growth triggers a wound healing response. Similar to wound healing, fibroblasts in the tumor stroma differentiate into myofibroblasts (also referred to as cancer-associated fibroblasts) primarily, but not exclusively, in response to transforming growth factor-β (TGF-β). Myofibroblasts in turn enhance tumor progression by remodeling the stroma. Among proteases implicated in stroma remodeling, matrix metalloproteinases (MMPs), including MMP-9, play a prominent role. Recent evidence indicates that MMP-9 recruitment to the tumor cell surface enhances tumor growth and invasion. In the present work, we addressed the potential relevance of MMP-9 recruitment to and activity at the surface of fibroblasts. We show that recruitment of MMP-9 to the fibroblast cell surface occurs through its fibronectin-like (FN) domain and that the molecule responsible for the recruitment is lysyl hydroxylase 3 (LH3). Functional assays suggest that both pro- and active MMP-9 trigger α-smooth muscle actin expression in cultured fibroblasts, reflecting myofibroblast differentiation, possibly as a result of TGF-β activation. Moreover, the recombinant FN domain inhibited both MMP-9-induced TGF-β activation and α-smooth muscle actin expression by displacing MMP-9 from the fibroblast cell surface. Together our results uncover LH3 as a new docking receptor of MMP-9 on the fibroblast cell surface and demonstrate that the MMP-9 FN domain is essential for the interaction. They also show that the recombinant FN domain inhibits MMP-9-induced TGF-β activation and fibroblast differentiation, providing a potentially attractive therapeutic reagent toward attenuating tumor progression where MMP-9 activity is strongly implicated.
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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.