ArticleThe Journal of biological chemistry2009
Matrix metalloproteinase-2-deficient fibroblasts exhibit an alteration in the fibrotic response to connective tissue growth factor/CCN2 because of an increase in the levels of endogenous fibronectin.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Role of CTGF-LRP1 in impaired healing of cesarean section incisions.Nature communications · 2026Article
- Genetically engineered biomimetic ATP-responsive nanozyme for the treatment of cardiac fibrosis.Journal of nanobiotechnology · 2025Article
- Efficacy of epidermal growth factor in suppressing inflammation and proliferation in pterygial fibroblasts through interactions with microenvironmental M1 macrophages.Scientific reports · 2024Article
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- Pro-Fibrotic Phenotype in a Patient with Segmental Stiff Skin Syndrome via TGF-β Signaling Overactivation.International journal of molecular sciences · 2020Article
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- A novel Fas-binding outer membrane protein and lipopolysaccharide of Leptospira interrogans induce macrophage apoptosis through the Fas/FasL-caspase-8/-3 pathway.Emerging microbes & infections · 2018Article
- Dual roles of tumour cells-derived matrix metalloproteinase 2 on brain tumour growth and invasion.British journal of cancer · 2017Article
- Upregulation of microRNA-4417 and Its Target Genes Contribute to Nickel Chloride-promoted Lung Epithelial Cell Fibrogenesis and Tumorigenesis.Scientific reports · 2017Article
- Regulatory mechanisms of anthrax toxin receptor 1-dependent vascular and connective tissue homeostasis.Matrix biology : journal of the International Society for Matrix Biology · 2015Article
- Understanding Fibroblasts in Order to Comprehend the Osteopathic Treatment of the Fascia.Evidence-based complementary and alternative medicine : eCAM · 2015Review
- RECK-Mediated β1-Integrin Regulation by TGF-β1 Is Critical for Wound Contraction in Mice.PloS one · 2015Article
- Kynurenine increases matrix metalloproteinase-1 and -3 expression in cultured dermal fibroblasts and improves scarring in vivo.The Journal of investigative dermatology · 2014Article
- Potent tumor targeting drug release system comprising MMP-2 specific peptide fragment with self-assembling characteristics.Drug design, development and therapy · 2014Article
- Breast tumor and stromal cell responses to TGF-β and hypoxia in matrix deposition.Matrix biology : journal of the International Society for Matrix Biology · 2013Review
- Article
- Loss of neuron-astroglial interaction rapidly induces protective CNTF expression after stroke in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Decorin interacts with connective tissue growth factor (CTGF)/CCN2 by LRR12 inhibiting its biological activity.The Journal of biological chemistry · 2011Article
- Integrin expression and function in the response of primary culture hepatic stellate cells to connective tissue growth factor (CCN2).Journal of cellular and molecular medicine · 2011Article
- AP-1 (Fra-1/c-Jun)-mediated induction of expression of matrix metalloproteinase-2 is required for 15S-hydroxyeicosatetraenoic acid-induced angiogenesis.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinase-2 (MMP-2) is an important extracellular matrix remodeling enzyme, and it has been involved in different fibrotic disorders. The connective tissue growth factor (CTGF/CCN2), which is increased in these pathologies, induces the production of extracellular matrix proteins. To understand the fibrotic process observed in diverse pathologies, we analyzed the fibroblast response to CTGF when MMP-2 activity is inhibited. CTGF increased fibronectin (FN) amount, MMP-2 mRNA expression, and gelatinase activity in 3T3 cells. When MMP-2 activity was inhibited either by the metalloproteinase inhibitor GM-6001 or in MMP-2-deficient fibroblasts, an increase in the basal amount of FN together with a decrease of its levels in response to CTGF was observed. This paradoxical effect could be explained by the fact that the excess of FN could block the access to other ligands, such as CTGF, to integrins. This effect was emulated in fibroblasts by adding exogenous FN or RGDS peptides or using anti-integrin alpha(V) subunit-blocking antibodies. Additionally, in MMP-2-deficient cells CTGF did not induce the formation of stress fibers, focal adhesion sites, and ERK phosphorylation. Anti-integrin alpha(V) subunit-blocking antibodies inhibited ERK phosphorylation in control cells. Finally, in MMP-2-deficient cells, FN mRNA expression was not affected by CTGF, but degradation of (125)I-FN was increased. These results suggest that expression, regulation, and activity of MMP-2 can play an important role in the initial steps of fibrosis and shows that FN levels can regulate the cellular response to CTGF.
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