PMID- 29263936
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240327
IS  - 2095-4700 (Print)
IS  - 2095-6231 (Electronic)
IS  - 2095-4700 (Linking)
VI  - 5
DP  - 2017
TI  - RANKL-induced M1 macrophages are involved in bone formation.
PG  - 17019
LID - 10.1038/boneres.2017.19 [doi]
AB  - The activation of M1 macrophages can be achieved by stimulating them with 
      lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). However, M1 can be found under 
      physiological conditions without any pathological stimuli. This study aimed to 
      understand the involvement of RANKL-induced M1 macrophages in bone formation 
      compared with pathologically induced macrophages. Fischer rats were used to 
      investigate macrophage distribution in normal and injured femoral condyles in 
      vivo. Bone marrow-derived macrophages (BMDMs) were activated with LPS+IFN-gamma and 
      RANKL to achieve M1 activation in vitro. Gene expression related to inflammation, 
      osteoclastogenesis, angiogenesis, and migration was determined by reverse 
      transcription-quantitative polymerase chain reaction (RT-qPCR) and 
      fluorescence-activated cell sorting (FACS). Tissue macrophages showed distinct 
      expression patterns at different bone regions. RANKL was found in close proximity 
      to inducible nitric oxide synthase-positive (iNOS+) cells in vivo, suggesting an 
      association between RANKL expression and iNOS+ cells, especially in trabecular 
      bone. RANKL-induced macrophages showed a different cytokine secretion profile 
      compared with pathologically induced macrophages. Both osteoclasts and M1 
      macrophages peaked on day 7 during bone healing. RANKL could trigger M1-like 
      macrophages with properties that were different from those of LPS+IFN-gamma-induced 
      macrophages. These RANKL-activated M1 macrophages were actively involved in bone 
      formation.
FAU - Huang, Rong
AU  - Huang R
AD  - The Institute of Health and Biomedical Innovation, Queensland University of 
      Technology, Brisbane, Queensland, Australia.
FAU - Wang, Xin
AU  - Wang X
AD  - The Institute of Health and Biomedical Innovation, Queensland University of 
      Technology, Brisbane, Queensland, Australia.
AD  - Department of Orthopaedic Surgery, Affiliated Hospital of Zunyi Medical 
      University, Zunyi, Guizhou, China.
FAU - Zhou, Yinghong
AU  - Zhou Y
AD  - The Institute of Health and Biomedical Innovation, Queensland University of 
      Technology, Brisbane, Queensland, Australia.
FAU - Xiao, Yin
AU  - Xiao Y
AD  - The Institute of Health and Biomedical Innovation, Queensland University of 
      Technology, Brisbane, Queensland, Australia.
LA  - eng
PT  - Journal Article
DEP - 20171017
PL  - China
TA  - Bone Res
JT  - Bone research
JID - 101608652
PMC - PMC5645773
COIS- The authors declare no conflict of interest.
EDAT- 2017/12/22 06:00
MHDA- 2017/12/22 06:01
PMCR- 2017/10/17
CRDT- 2017/12/22 06:00
PHST- 2016/07/02 00:00 [received]
PHST- 2016/12/20 00:00 [revised]
PHST- 2017/02/15 00:00 [accepted]
PHST- 2017/12/22 06:00 [entrez]
PHST- 2017/12/22 06:00 [pubmed]
PHST- 2017/12/22 06:01 [medline]
PHST- 2017/10/17 00:00 [pmc-release]
AID - boneres201719 [pii]
AID - 10.1038/boneres.2017.19 [doi]
PST - epublish
SO  - Bone Res. 2017 Oct 17;5:17019. doi: 10.1038/boneres.2017.19. eCollection 2017.