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    Enhanced fracture repair by leukotriene antagonism is characterized by increased chondrocyte proliferation and early bone formation: a novel role of the cysteinyl LT-1 receptor

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    Authors
    Wixted, John J.
    Fanning, Paul J.
    Gaur, Tripti
    O'Connell, Shannon L.
    Silva, Jason
    Mason-Savas, April
    Ayers, David C.
    Stein, Gary S.
    Lian, Jane B.
    UMass Chan Affiliations
    Department of Orthopedic Surgery and Physical Rehabilitation
    Department of Cell Biology
    Department of Orthopedics
    Document Type
    Journal Article
    Publication Date
    2009-10-23
    Keywords
    Acetates
    Animals
    Arachidonate 5-Lipoxygenase
    Cell Proliferation
    Chondrocytes
    Fracture Healing
    Fractures, Bone
    Gene Expression Regulation
    Hydroxyurea
    Hypertrophy
    Leukotriene Antagonists
    Leukotriene B4
    Mice
    Models, Biological
    Osteogenesis
    Quinolines
    Receptors, Leukotriene
    Cell Biology
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    Link to Full Text
    http://dx.doi.org/10.1002/jcp.21809
    Abstract
    Inflammatory mediators and drugs which affect inflammation can influence the healing of injured tissues. Leukotrienes are potent inflammatory mediators, and similar to prostaglandins, are metabolites of arachidonic acid which can have positive or negative effects on bone and cartilage tissues. Here we tested the hypothesis that blocking the negative regulation of leukotrienes, would lead to enhanced endochondral bone formation during fracture repair. A closed femoral fracture was created in mice. Animals were divided into three groups for treatment with either montelukast sodium, a cysteinyl leukotriene type 1 receptor antagonist (trade name Singulair), zileuton, a 5-lipoxygenase enzyme inhibitor (trade name Zyflo), or carrier alone. The fractures were analyzed using radiographs, quantitative gene expression, histology and histomorphometry, and immunohistochemistry. Both the montelukast sodium group and the zileuton group exhibited enhanced fracture repair when compared with controls. Both treatment groups exhibited increased callous size and earlier bone formation when compared to controls as early as day 7. Gene expression analysis of treatment groups showed increased markers of chondrocyte proliferation and differentiation, and increased early bone formation markers when compared with controls. Treatment with montelukast sodium directly targeted the cysteinyl leukotriene type 1 receptor, leading to increased chondrocyte proliferation at early time points. These novel findings suggests a potential mechanism by which the cysteinyl leukotriene type 1 receptor acts as a negative regulator of chondrocyte proliferation, with important and previously unrecognized implications for both fracture repair, and in a broader context, systemic chondrocyte growth and differentiation.
    Source
    J Cell Physiol. 2009 Oct;221(1):31-9. Link to article on publisher's site
    DOI
    10.1002/jcp.21809
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/49604
    PubMed ID
    19544365
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1002/jcp.21809
    Scopus Count
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