Document Detail

Genetic and cellular evidence of decreased inflammation associated with reduced incidence of posttraumatic arthritis in MRL/MpJ mice.
MedLine Citation:
PMID:  23203659     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To examine the relationship between inflammation and posttraumatic arthritis (PTA) in a murine intraarticular fracture model.
METHODS: Male C57BL/6 and MRL/MpJ "superhealer" mice received tibial plateau fractures using a previously established method. Mice were killed on day 0 (within 4 hours of fracture) and days 1, 3, 5, 7, 28, and 56 after fracture. Synovial tissue samples, obtained prior to fracture and on days 0, 1, 3, 5, and 7 after fracture, were examined by reverse transcription-polymerase chain reaction for gene expression of proinflammatory cytokines and chemokines. Synovial fluid and serum samples were collected to measure cytokine concentrations, using enzyme-linked immunosorbent assay. Whole joints were examined histologically for the extent of synovitis and cartilage degradation, and joint tissue samples from all time points were analyzed immunohistochemically to evaluate the distribution of interleukin-1 (IL-1).
RESULTS: Compared to C57BL/6 mice, MRL/MpJ mice had less severe intraarticular and systemic inflammation following joint injury, as evidenced by lower gene expression of tumor necrosis factor α and IL-1β in the synovial tissue and lower protein levels of IL-1α and IL-1β in the synovial fluid, serum, and joint tissues. Furthermore, after joint injury, MRL/MpJ mice had lower gene expression of macrophage inflammatory proteins and macrophage-derived chemokine (CCL22) in the synovial tissue, and also had reduced acute and late-stage infiltration of synovial macrophages.
CONCLUSION: C57BL/6 mice exhibited higher levels of inflammation than MRL/MpJ mice, indicating that MRL/MpJ mice are protected from PTA in this model. These data thus suggest an association between joint tissue inflammation and the development and progression of PTA in mice.
John S Lewis; Bridgette D Furman; Evan Zeitler; Janet L Huebner; Virginia B Kraus; Farshid Guilak; Steven A Olson
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arthritis and rheumatism     Volume:  65     ISSN:  1529-0131     ISO Abbreviation:  Arthritis Rheum.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-02-26     Completed Date:  2013-04-24     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  0370605     Medline TA:  Arthritis Rheum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  660-70     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2013 by the American College of Rheumatology.
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MeSH Terms
Arthritis / epidemiology,  genetics*,  immunology
Chemokines / genetics,  immunology
Disease Models, Animal
Fracture Healing / genetics*,  immunology
Interleukin-1alpha / genetics*,  immunology
Interleukin-1beta / genetics*,  immunology
Macrophages / immunology
Mice, Inbred C57BL
Mice, Inbred MRL lpr
Species Specificity
Synovial Membrane / immunology
Synovitis / epidemiology,  genetics,  immunology
Tibial Fractures / epidemiology,  genetics*,  immunology
Tumor Necrosis Factor-alpha / genetics*,  immunology
Grant Support
AG-15768/AG/NIA NIH HHS; AR-48182/AR/NIAMS NIH HHS; AR-48852/AR/NIAMS NIH HHS; AR-50245/AR/NIAMS NIH HHS; P01 AR050245/AR/NIAMS NIH HHS; R01 AG015768/AG/NIA NIH HHS; R01 AR048182/AR/NIAMS NIH HHS; R01 AR048852/AR/NIAMS NIH HHS; //Howard Hughes Medical Institute
Reg. No./Substance:
0/Chemokines; 0/Interleukin-1alpha; 0/Interleukin-1beta; 0/Tumor Necrosis Factor-alpha

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