ArticleArthritis & rheumatology (Hoboken, N.J.)2015
Lubricin restoration in a mouse model of congenital deficiency.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Lubricin in experimental and naturally occurring osteoarthritis: a systematic review.Osteoarthritis and cartilage · 2020Pooled it
- O-GlcNAcylation as a Metabolic Integrator in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2026Review
- PRG4-Related Camptodactyly-Arthropathy-Coxa Vara-Pericarditis Syndrome Mimicking Juvenile Idiopathic Arthritis: A Case-Based Review.International journal of molecular sciences · 2026Article
- Disruption of proteoglycan 4 (PRG4)-CD44 signaling modulates chronic synovitis in conditionally inactivated mice.Arthritis research & therapy · 2026Article
- Proteoglycan-4 (PRG4) serum concentration is lower in aged mice, and genetic deficiency impacts survival probability, blood parameters, and bone during aging.GeroScience · 2026Article
- Delayed Lubricin Injection Improves Cartilage Repair Tissue Quality in an In Vivo Rabbit Osteochondral Defect Model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Disruption of Proteoglycan 4 (PRG4)-CD44 Signaling Modulates Chronic Synovitis in Conditionally Inactivated Mice.Research square · 2025Article
- A major functional role of synovial fluid is to reduce the rate of cartilage fatigue failure under cyclical compressive loading.Osteoarthritis and cartilage · 2025Article
- Proteoglycan 4 (Lubricin) and regulation of xanthine oxidase in synovial macrophage as a mechanism of controlling synovitis.Arthritis research & therapy · 2024Article
- Proteoglycan 4 (Lubricin) and Regulation of Xanthine Oxidase in Synovial Macrophage as A Mechanism of Controlling Synovitis.Research square · 2024Article
- Quadruped Gait and Regulation of Apoptotic Factors in Tibiofemoral Joints following Intra-Articular rhPRG4 Injection inInternational journal of molecular sciences · 2022Article
- Proteoglycan-4 is an essential regulator of synovial macrophage polarization and inflammatory macrophage joint infiltration.Arthritis research & therapy · 2021Article
- Recombinant Human Proteoglycan 4 Regulates Phagocytic Activation of Monocytes and Reduces IL-1β Secretion by Urate Crystal Stimulated Gout PBMCs.Frontiers in immunology · 2021Article
- Proteoglycan-4 regulates fibroblast to myofibroblast transition and expression of fibrotic genes in the synovium.Arthritis research & therapy · 2020Article
- Lubricin as a Therapeutic and Potential Biomarker in Sepsis.Critical care clinics · 2020Review
- The Roles of Indian Hedgehog Signaling in TMJ Formation.International journal of molecular sciences · 2019Review
- Mechanisms of synovial joint and articular cartilage development.Cellular and molecular life sciences : CMLS · 2019Review
- Recombinant human proteoglycan-4 reduces phagocytosis of urate crystals and downstream nuclear factor kappa B and inflammasome activation and production of cytokines and chemokines in human and murine macrophages.Arthritis research & therapy · 2018Article
- Early genetic restoration of lubricin expression in transgenic mice mitigates chondrocyte peroxynitrite release and caspase-3 activation.Osteoarthritis and cartilage · 2017Article
- Friction-Induced Mitochondrial Dysregulation Contributes to Joint Deterioration in Prg4 Knockout Mice.International journal of molecular sciences · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveCongenital deficiency of the principal boundary lubricant in cartilage (i.e., lubricin, encoded by the gene PRG4) increases joint friction and causes progressive joint failure. This study was undertaken to determine whether restoring lubricin expression in a mouse model would prevent, delay, or reverse the disease process caused by congenital deficiency.
methodsUsing genetically engineered lubricin-deficient mice, we restored gene function before conception or at ages 3 weeks, 2 months, or 6 months after birth. The effect of restoring gene function (i.e., expression of lubricin) on the tibiofemoral patellar joints of mice was evaluated histologically and by ex vivo biomechanical testing.
resultsRestoring gene function in mice prior to conception prevented joint disease. In 3-week-old mice, restoring gene function improved, but did not normalize, histologic features of the articular cartilage and whole-joint friction. In addition, cyclic loading of the joints produced fewer activated caspase 3-containing chondrocytes when lubricin expression was restored, as compared to that in littermate mice whose gene function was not restored (nonrestored controls). Restoration of lubricin expression in 2-month-old or 6-month-old mice had no beneficial effect on histopathologic cartilage damage, extent of whole-joint friction, or activation of caspase 3 when compared to nonrestored controls.
conclusionWhen boundary lubrication is congenitally deficient and cartilage becomes damaged, the window of opportunity for restoring lubrication and slowing disease progression is limited.
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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.