ArticleThe Journal of clinical investigation2005
Synergy between a plasminogen cascade and MMP-9 in autoimmune disease.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 110 citations in OpenAlex.
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- Matrix Metalloproteinases in Inflammatory Dermatoses.International journal of molecular sciences · 2025Review
- BDNF-driven synaptic plasticity requires autocrine matrix metalloproteinase-9 activity.Science advances · 2025Article
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- Dissection of the signal transduction machinery responsible for the lysyl oxidase-like 4-mediated increase in invasive motility in triple-negative breast cancer cells: mechanistic insight into the integrin-β1-NF-κB-MMP9 axis.Frontiers in oncology · 2024Article
- The Eotaxin-1/CCR3 Axis and Matrix Metalloproteinase-9 Are Critical in Anti-NC16A IgE-Induced Bullous Pemphigoid.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Fibrotic remodeling and tissue regeneration mechanisms define the therapeutic potential of human muscular progenitors.Bioengineering & translational medicine · 2023Article
- Pruritogens in pemphigoid diseases: Possible therapeutic targets for a burdensome symptom.The Journal of dermatology · 2023Review
- Insights Into the Pathogenesis of Bullous Pemphigoid: The Role of Complement-Independent Mechanisms.Frontiers in immunology · 2022Review
- A Scoping Review of the Role of Metalloproteinases in the Pathogenesis of Autoimmune Pemphigus and Pemphigoid.Biomolecules · 2021Article
- Granzyme B inhibition reduces disease severity in autoimmune blistering diseases.Nature communications · 2021Article
- Immune Mechanism, Gene Module, and Molecular Subtype Identification of Astragalus Membranaceus in the Treatment of Dilated Cardiomyopathy: An Integrated Bioinformatics Study.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- A type IV collagenase inhibitor, N-hydroxy-3-phenyl-2-(4-phenylbenzenesulfonamido) propanamide (BiPS), suppresses skin injury induced by sulfur mustard.Toxicology and applied pharmacology · 2020Article
- Relief of tumor hypoxia unleashes the tumoricidal potential of neutrophils.The Journal of clinical investigation · 2020Article
- Resolution in bullous pemphigoid.Seminars in immunopathology · 2019Review
- NET Formation in Bullous Pemphigoid Patients With Relapse Is Modulated by IL-17 and IL-23 Interplay.Frontiers in immunology · 2019Observational
- Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019Review
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6 authors at 3 institutions in 1 country.
Funding
Abstract
Extracellular proteolysis by the plasminogen/plasmin (Plg/plasmin) system and MMPs is required for tissue injury in autoimmune and inflammatory diseases. We demonstrate that a Plg cascade synergizes with MMP-9/gelatinase B in vivo during dermal-epidermal separation in an experimental model of bullous pemphigoid (BP), an autoimmune disease. BP was induced in mice by antibodies to the hemidesmosomal antigen BP180. Mice deficient in MMP-9 were resistant to experimental BP, while mice deficient in Plg and both tissue Plg activator (tPA) and urokinase Plg activator (uPA) showed delayed and less intense blister formation induced by antibodies to BP180. Plg-deficient mice reconstituted locally with Plg or the active form of MMP-9 (actMMP-9), but not the proenzyme form of MMP-9 (proMMP-9), developed BP. In contrast, proMMP-9 or actMMP-9, but not Plg, reconstituted susceptibility of MMP-9-deficient mice to the skin disease. In addition, MMP-3-deficient mice injected with pathogenic IgG developed the same degree of BP and expressed levels of actMMP-9 in the skin similar to those of WT controls. Thus, the Plg/plasmin system is epistatic to MMP-9 activation and subsequent dermal-epidermal separation in BP.
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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.