ArticleArthritis & rheumatology (Hoboken, N.J.)2018
Role of ADAMTS-12 in Protecting Against Inflammatory Arthritis in Mice By Interacting With and Inactivating Proinflammatory Connective Tissue Growth Factor.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Nerve growth factor receptor limits inflammation to promote remodeling and repair of osteoarthritic joints.Nature communications · 2024Article
- Lung Inflammatory Phenotype in Mice Deficient in Fibulin-2 and ADAMTS-12.International journal of molecular sciences · 2024Article
- Nerve Growth Factor Receptor Limits Inflammation to Promote Remodeling and Repair of Osteoarthritic Joints.bioRxiv : the preprint server for biology · 2023Article
- Achilles' Heel-The Significance of Maintaining Microenvironmental Homeostasis in the Nucleus Pulposus for Intervertebral Discs.International journal of molecular sciences · 2023Review
- Tau deficiency inhibits classically activated macrophage polarization and protects against collagen-induced arthritis in mice.Arthritis research & therapy · 2023Article
- Phylogenetic inference of the emergence of sequence modules and protein-protein interactions in the ADAMTS-TSL family.PLoS computational biology · 2023Article
- TAILS Identifies Candidate Substrates and Biomarkers of ADAMTS7, a Therapeutic Protease Target in Coronary Artery Disease.Molecular & cellular proteomics : MCP · 2022Article
- CTGF as a multifunctional molecule for cartilage and a potential drug for osteoarthritis.Frontiers in endocrinology · 2022Review
- The protein-protein interaction between connective tissue growth factor and annexin A2 is relevant to pannus formation in rheumatoid arthritis.Arthritis research & therapy · 2021Article
- Diagnostic value of serum connective tissue growth factor in rheumatoid arthritis.Clinical rheumatology · 2021Article
- Progranulin promotes bone fracture healing via TNFR pathways in mice with type 2 diabetes mellitus.Annals of the New York Academy of Sciences · 2021Article
- Fexofenadine Protects Against Intervertebral Disc Degeneration Through TNF Signaling.Frontiers in cell and developmental biology · 2021Article
- ADAMTS-12: Functions and Challenges for a Complex Metalloprotease.Frontiers in molecular biosciences · 2021Review
- Follistatin-Like 1 Attenuation Suppresses Intervertebral Disc Degeneration in Mice through Interacting with TNF-Oxidative medicine and cellular longevity · 2021Article
- Dynamic Change of Lumbar Structure and Associated Factors: A Retrospective Study.Orthopaedic surgery · 2019Article
- Progranulin Is Positively Associated with Intervertebral Disc Degeneration by Interaction with IL-10 and IL-17 Through TNF Pathways.Inflammation · 2018Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveIt has been reported that ADAMTS-12 is a susceptibility gene for rheumatoid arthritis (RA) development, and its level is significantly increased in RA patients. In addition, ADAMTS-12 is reported to be required for inflammation in otherwise healthy subjects. This study was undertaken to determine the role of ADAMTS-12 and the underlying mechanisms in the pathogenesis of inflammatory arthritis.
methodsThe collagen-induced arthritis (CIA) model was established in ADAMTS-12-deficient mice and their control littermates to determine the role of ADAMTS-12 in vivo. Micro-computed tomography scanning was used to demonstrate the destruction of the ankle joint; histologic analysis illustrated synovitis, pannus formation, and bone and cartilage destruction; enzyme-linked immunosorbent assay was performed to measure serum levels of inflammatory cytokines; and protein-protein interaction assays were performed to detect the interactions of ADAMTS-12 and its various deletion mutants with connective tissue growth factor (CTGF).
resultsDeficiency of ADAMTS-12 led to accelerated inflammatory arthritis in the CIA mouse model. Loss of ADAMTS-12 caused enhanced osteoclastogenesis. In vitro and in vivo protein-protein interaction assays demonstrated that ADAMTS-12 bound and processed CTGF, a previously unrecognized substrate of ADAMTS-12. In addition, deletion of ADAMTS-12 enhanced, while overexpression of ADMATS-12 reduced, CTGF-mediated inflammation. Furthermore, ADAMTS-12 regulation of inflammation was largely lost in CTGF-deficient macrophages. Importantly, blocking of CTGF attenuated elevated inflammatory arthritis seen in the ADAMTS-12-deficient CIA mouse model.
conclusionThis study provides evidence that ADAMTS-12 is a critical regulator of inflammatory arthritis and that this is mediated, at least in part, through control of CTGF turnover.
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