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dc.contributor.authorBatoon, Lena
dc.contributor.authorMillard, Susan Marie
dc.contributor.authorWullschleger, Martin Eduard
dc.contributor.authorPreda, Corina
dc.contributor.authorWu, Andy Chiu-Ku
dc.contributor.authorKaur, Simranpreet
dc.contributor.authorTseng, Hsu-Wen
dc.contributor.authorHume, David Arthur
dc.contributor.authorLevesque, Jean-Pierre
dc.contributor.authorRaggatt, Liza Jane
dc.contributor.authorPettit, Allison Robyn
dc.date.accessioned2018-05-02T04:34:05Z
dc.date.available2018-05-02T04:34:05Z
dc.date.issued2019
dc.identifier.issn0142-9612
dc.identifier.doi10.1016/j.biomaterials.2017.10.033
dc.identifier.urihttp://hdl.handle.net/10072/374334
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.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherElsevier
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto16
dc.relation.ispartofjournalBiomaterials
dc.subject.fieldofresearchClinical Sciences not elsewhere classified
dc.subject.fieldofresearchcode110399
dc.titleCD169+ macrophages are critical for osteoblast maintenance and promote intramembranous and endochondral ossification during bone repair
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.description.notepublicThis publication has been entered into Griffith Research Online as an Advanced Online Version.
gro.hasfulltextNo Full Text
gro.griffith.authorWullschleger, Martin


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