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Title: | CD169+ macrophages are critical for osteoblast maintenance and promote intramembranous and endochondral ossification during bone repair | Authors: | 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 |
Issue Date: | Mar-2019 | Publisher: | Elsevier | Source: | Biomaterials. 2019 Mar;196:51-66. doi: 10.1016/j.biomaterials.2017.10.033. Epub 2017 Oct 22. | Journal: | Biomaterials | 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 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. | DOI: | 10.1016/j.biomaterials.2017.10.033 | Keywords: | bone structure;fracture treatment;macrophage;Osteoblast | Type: | Article |
Appears in Sites: | Metro North HHS Publications |
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