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  • CD169+ macrophages are critical for osteoblast maintenance and promote intramembranous and endochondral ossification during bone repair

    Author(s)
    Batoon, Lena
    Millard, Susan Marie
    Wullschleger, Martin Eduard
    Preda, Corina
    Wu, Andy Chiu-Ku
    Kaur, Simranpreet
    Tseng, Hsu-Wen
    Hume, David Arthur
    Levesque, Jean-Pierre
    Raggatt, Liza Jane
    Pettit, Allison Robyn
    Griffith University Author(s)
    Wullschleger, Martin
    Year published
    2019
    Metadata
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    Abstract
    Osteal macrophages (osteomacs) contribute to bone homeostasis and regeneration. To further distinguish their functions from osteoclasts, which share many markers and growth factor requirements, we developed a rapid, enzyme-free osteomac enrichment protocol that permitted characterization of minimally manipulated osteomacs by flow cytometry. Osteomacs differ from osteoclasts in expression of Siglec1 (CD169). This distinction was confirmed using the CD169-diphtheria toxin (DT) receptor (DTR) knock-in model. DT treatment of naïve CD169-DTR mice resulted in selective and striking loss of osteomacs, whilst osteoclasts and trabecular ...
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    Osteal macrophages (osteomacs) contribute to bone homeostasis and regeneration. To further distinguish their functions from osteoclasts, which share many markers and growth factor requirements, we developed a rapid, enzyme-free osteomac enrichment protocol that permitted characterization of minimally manipulated osteomacs by flow cytometry. Osteomacs differ from osteoclasts in expression of Siglec1 (CD169). This distinction was confirmed using the CD169-diphtheria toxin (DT) receptor (DTR) knock-in model. DT treatment of naïve CD169-DTR mice resulted in selective and striking loss of osteomacs, whilst osteoclasts and trabecular bone area were unaffected. Consistent with a previously-reported trophic interaction, osteomac loss was accompanied by a concomitant and proportionately striking reduction in osteoblasts. The impact of CD169+ macrophage depletion was assessed in two models of bone injury that heal via either intramembranous (tibial injury) or endochondral (internally-plated femoral fracture model) ossification. In both models, CD169+ macrophage, including osteomac depletion compromised bone repair. Importantly, DT treatment in CD169-DTR mice did not affect osteoclast frequency in either model. In the femoral fracture model, the magnitude of callus formation correlated with the number of F4/80+ macrophages that persisted within the callus. Overall these observations provide compelling support that CD169+ osteomacs, independent of osteoclasts, provide vital pro-anabolic support to osteoblasts during both bone homeostasis and repair.
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    Journal Title
    Biomaterials
    DOI
    https://doi.org/10.1016/j.biomaterials.2017.10.033
    Note
    This publication has been entered into Griffith Research Online as an Advanced Online Version.
    Subject
    Clinical Sciences not elsewhere classified
    Publication URI
    http://hdl.handle.net/10072/374334
    Collection
    • Journal articles

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