Temporal and spatial expression of osteoactivin during fracture repair

Authors

  • Samir M. Abdelmagid,

    1. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania
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  • Mary F. Barbe,

    1. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania
    2. Department of Physical Therapy, Temple University, Philadelphia, Pennsylvania
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  • Michael Hadjiargyrou,

    1. Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York
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  • Thomas A. Owen,

    1. Theoretical and Applied Science, Ramapo College of New Jersey, Mahwah, New Jersey
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  • Roshanak Razmpour,

    1. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania
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  • Saqib Rehman,

    1. Department of Orthopaedic Surgery and Sports Medicine, Temple University Hospitals, Philadelphia, Pennsylvania
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  • Steven N. Popoff,

    1. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania
    2. Department of Orthopaedic Surgery and Sports Medicine, Temple University Hospitals, Philadelphia, Pennsylvania
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  • Fayez F. Safadi

    Corresponding author
    1. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania
    2. Department of Orthopaedic Surgery and Sports Medicine, Temple University Hospitals, Philadelphia, Pennsylvania
    3. Department of Otolaryngology—Head and Neck Surgery, Temple University Hospitals, Philadelphia, Pennsylvania
    • Associate Professor, Vice Chairperson for Research, Department of Anatomy and Cell Biology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140.
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  • The authors have no conflict of interest.

Abstract

We previously identified osteoactivin (OA) as a novel secreted osteogenic factor with high expression in developing long bones and calvaria, and that stimulates osteoblast differentiation and matrix mineralization in vitro. In this study, we report on OA mRNA and protein expression in intact long bone and growth plate, and in fracture calluses collected at several time points up to 21 days post-fracture (PF). OA mRNA and protein were highly expressed in osteoblasts localized in the metaphysis of intact tibia, and in hypertrophic chondrocytes localized in growth plate, findings assessed by in situ hybridization and immunohistochemistry, respectively. Using a rat fracture model, Northern blot analysis showed that expression of OA mRNA was significantly higher in day-3 and day-10 PF calluses than in intact rat femurs. Using in situ hybridization, we examined OA mRNA expression during fracture healing and found that OA was temporally regulated, with positive signals seen as early as day-3 PF, reaching a maximal intensity at day-10 PF, and finally declining at day-21 PF. At day-5 PF, which correlates with chondrogenesis, OA mRNA levels were significantly higher in the soft callus than in intact femurs. Similarly, we detected high OA protein immunoexpression throughout the reparative phase of the hard callus compared to intact femurs. Interestingly, the secreted OA protein was also detected within the newly made cartilage matrix and osteoid tissue. Taken together, these results suggest the possibility that OA plays an important role in bone formation and serves as a positive regulator of fracture healing. J. Cell. Biochem. 111: 295–309, 2010. © 2010 Wiley-Liss, Inc.

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