ArticleBlood advances2017
Urokinase plasminogen activator and receptor promote collagen-induced arthritis through expression in hematopoietic cells.
Article in Blood advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Review
- Transcriptomic signatures of classical monocytes reveal pro-inflammatory modules and heterogeneity in polyarticular juvenile idiopathic arthritis.Frontiers in immunology · 2024Article
- Allometrically scaling tissue forces drive pathological foreign-body responses to implants via Rac2-activated myeloid cells.Nature biomedical engineering · 2023Article
- Targeted imaging of uPAR expression in vivo with cyclic AE105 variants.Scientific reports · 2023Article
- Maintaining the balance: the critical role of plasmin activity in orthopedic surgery injury response.Journal of thrombosis and haemostasis : JTH · 2023Review
- Article
- The potential role of protease systems in hemophilic arthropathy.Blood advances · 2022Article
- Myricitrin inhibits fibroblast-like synoviocyte-mediated rheumatoid synovial inflammation and joint destruction by targeting AIM2.Frontiers in pharmacology · 2022Article
- Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Targeting the Urokinase-Type Plasminogen Activator Receptor (uPAR) in Human Diseases With a View to Non-invasive Imaging and Therapeutic Intervention.Frontiers in cell and developmental biology · 2021Review
- Molecular imaging of the urokinase plasminogen activator receptor: opportunities beyond cancer.EJNMMI research · 2020Review
- Article
- Plasminogen activation in the musculoskeletal acute phase response: Injury, repair, and disease.Research and practice in thrombosis and haemostasis · 2020Review
- Identification and preclinical development of an anti-proteolytic uPA antibody for rheumatoid arthritis.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Evolution and Medical Significance of LU Domain-Containing Proteins.International journal of molecular sciences · 2019Review
- Did evolution create a flexible ligand-binding cavity in the urokinase receptor through deletion of a plesiotypic disulfide bond?The Journal of biological chemistry · 2019Article
- The Urokinase Plasminogen Activation System in Rheumatoid Arthritis: Pathophysiological Roles and Prospective Therapeutic Targets.Current drug targets · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The plasminogen activation (PA) system has been implicated in driving inflammatory arthritis, but the precise contribution of PA system components to arthritis pathogenesis remains poorly defined. Here, the role of urokinase plasminogen activator (uPA) and its cognate receptor (uPAR) in the development and severity of inflammatory joint disease was determined using uPA- and uPAR-deficient mice inbred to the strain DBA/1J, a genetic background highly susceptible to collagen-induced arthritis (CIA). Mice deficient in uPA displayed a near-complete amelioration of macroscopic and histological inflammatory joint disease following CIA challenge. Similarly, CIA-challenged uPAR-deficient mice exhibited significant amelioration of arthritis incidence and severity. Reduced disease development in uPA-deficient and uPAR-deficient mice was not due to an altered adaptive immune response to the CIA challenge. Reciprocal bone marrow transplant studies indicated that uPAR-driven CIA was due to expression by hematopoietic-derived cells, as mice with uPAR-deficient bone marrow challenged with CIA developed significantly reduced macroscopic and histological joint disease as compared with mice with uPAR expression limited to non-hematopoietic-derived cells. These findings indicate a fundamental role for uPAR-expressing hematopoietic cells in driving arthritis incidence and progression. Thus, uPA/uPAR-mediated cell surface proteolysis and/or uPAR-mediated signaling events promote inflammatory joint disease, indicating that disruption of this key proteolytic/signaling system may provide a novel therapeutic strategy to limit clinical arthritis.
Identifiers
What OpenQuestion holds
Registered trials
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.