RANKL-induced M1 macrophages are involved in bone formation.
RANKL-induced M1 macrophages are involved in bone formation.
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DOI:
10.1038/boneres.2017.19
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发表时间:
2017
期刊:
影响因子:
12.7
通讯作者:
Xiao Y
中科院分区:
文献类型:
--
作者:
Huang R;Wang X;Zhou Y;Xiao Y
The activation of M1 macrophages can be achieved by stimulating them with lipopolysaccharide (LPS) and interferon-γ (IFN-γ). 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-γ 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-γ-induced macrophages. These RANKL-activated M1 macrophages were actively involved in bone formation.
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影响因子:
3.7
作者:
Jablonski KA;Amici SA;Webb LM;Ruiz-Rosado Jde D;Popovich PG;Partida-Sanchez S;Guerau-de-Arellano M
通讯作者:
Guerau-de-Arellano M
影响因子:
9.3
作者:
Cherry JD;Olschowka JA;O'Banion MK
通讯作者:
O'Banion MK
DOI:
10.1084/jem.176.1.287
发表时间:
1992-07-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Stein M;Keshav S;Harris N;Gordon S
通讯作者:
Gordon S
影响因子:
6.2
作者:
Alexander, Kylie A.;Chang, Ming K.;Pettit, Allison R.
通讯作者:
Pettit, Allison R.
影响因子:
7.5
作者:
Loi F;Córdova LA;Zhang R;Pajarinen J;Lin TH;Goodman SB;Yao Z
通讯作者:
Yao Z