Please use this identifier to cite or link to this item: https://dora.health.qld.gov.au/qldresearchjspui/handle/1/932
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dc.contributor.authorBatoon, Lenaen
dc.contributor.authorMillard, Susan Marieen
dc.contributor.authorWullschleger, Martin Eduarden
dc.contributor.authorPreda, Corinaen
dc.contributor.authorWu, Andy Chiu-Kuen
dc.contributor.authorKaur, Simranpreeten
dc.contributor.authorTseng, Hsu-Wenen
dc.contributor.authorHume, David Arthuren
dc.contributor.authorLevesque, Jean-Pierreen
dc.contributor.authorRaggatt, Liza Janeen
dc.contributor.authorPettit, Allison Robynen
dc.date.accessioned2019-05-30T01:36:08Z-
dc.date.available2019-05-30T01:36:08Z-
dc.date.issued2019-03-
dc.identifier.citationBiomaterials. 2019 Mar;196:51-66. doi: 10.1016/j.biomaterials.2017.10.033. Epub 2017 Oct 22.en
dc.identifier.urihttp://dora.health.qld.gov.au/qldresearchjspui/handle/1/932-
dc.description.abstractOsteal 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.en
dc.language.isoenen
dc.publisherElsevieren
dc.relation.ispartofBiomaterialsen
dc.subjectbone structureen
dc.subjectfracture treatmenten
dc.subjectmacrophageen
dc.subjectOsteoblasten
dc.titleCD169+ macrophages are critical for osteoblast maintenance and promote intramembranous and endochondral ossification during bone repairen
dc.typeArticleen
dc.identifier.doi10.1016/j.biomaterials.2017.10.033-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
Appears in Sites:Metro North HHS Publications
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