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موضوع: Adult Cartilage-Specific Peroxisome Proliferatore Activated Receptor Gamma Knockout Mice Exhibit the Spontaneous Osteoarthritis Phenotype

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    تاریخ عضویت
    Jul 2009
    رشته
    مهندسی شیمی
    نوشته ها
    514

    پیش فرض Adult Cartilage-Specific Peroxisome Proliferatore Activated Receptor Gamma Knockout Mice Exhibit the Spontaneous Osteoarthritis Phenotype

    Osteoarthritis (OA) is an age-related progressive degenerative joint disease. Peroxisome proliferatoreactivated
    receptor gamma (PPARg), a transcription factor, is suggested as an attractive
    therapeutic target to counteract degradative mechanisms associated with OA. Studies suggest that
    activation of PPARg by its agonists can reduce the synthesis of OA catabolic and inflammatory factors
    and the development of cartilage lesions in OA animal models. Because these agonists impart several
    PPARg-independent effects, the specific in vivo function of PPARg in cartilage homeostasis and OA
    remains largely unknown. Herein, we describe the in vivo role of PPARg in OA using cartilage-specific
    PPARg knockout (KO) mice generated using the Cre-lox system. Adult PPARg KO mice exhibited
    a spontaneous OA phenotype associated with enhanced cartilage degradation, hypocellularity,
    synovial and cartilage fibrosis, synovial inflammation, mononuclear cell influx in the synovium, and
    increased expression of catabolic factors, including matrix metalloproteinase-13, accompanied by an
    increase in staining for matrix metalloproteinaseegenerated aggrecan and type II collagen neoepitopes
    (VDIPEN and C1-2C). We demonstrate that PPARg-deficient articular cartilage exhibits
    elevated expression of the additional catabolic factors hypoxia-inducible factor-2a, syndecan-4, and
    a disintegrin and metalloproteinase with thrombospondin motifs 5 and of the inflammatory factors
    cyclooxygenase-2 and inducible nitric oxide synthase. In conclusion, PPARg is a critical regulator of
    cartilage health, the lack of which leads to an accelerated spontaneous OA phenotype. (Am J Pathol
    2013, 182: 1099e1106; Elsevier: Article Locator)
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