MCP-1 Is Induced by Receptor Activator of Nuclear Factor-κB Ligand, Promotes Human Osteoclast Fusion, and Rescues Granulocyte Macrophage Colony-stimulating Factor Suppression of Osteoclast Formation*

  title={MCP-1 Is Induced by Receptor Activator of Nuclear Factor-$\kappa$B Ligand, Promotes Human Osteoclast Fusion, and Rescues Granulocyte Macrophage Colony-stimulating Factor Suppression of Osteoclast Formation*},
  author={Michael Soo Ho Kim and Chris J Day and Nigel Alexander Morrison},
  journal={Journal of Biological Chemistry},
  pages={16163 - 16169}
Human osteoclast formation from monocyte precursors under the action of receptor activator of nuclear factor-κB ligand (RANKL) was suppressed by granulocyte macrophage colony-stimulating factor (GM-CSF), with down-regulation of critical osteoclast-related nuclear factors. GM-CSF in the presence of RANKL and macrophage colony-stimulating factor resulted in mononuclear cells that were negative for tartrate-resistant acid phosphatase (TRAP) and negative for bone resorption. CD1a, a dendritic cell… 

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Monocyte Chemotactic Protein-1 (MCP1) Accumulation in Human Osteoclast Precursor Cultures
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Dominant Negative MCP‐1 Blocks Human Osteoclast Differentiation
It is shown that a cascade of gene expression leading to osteoclast differentiation depends on intact early MCP‐1 induction and signaling in human osteoclasts, and that marker genes for osteOClast function cathepsin K and tartrate resistance acid phosphatase were maximally induced at 14 days, corresponding with mature osteoc last function.
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MCP-1 expressed by osteoclasts stimulates osteoclastogenesis in an autocrine/paracrine manner.
Formononetin attenuates osteoclastogenesis via suppressing the RANKL-induced activation of NF-κB, c-Fos, and nuclear factor of activated T-cells cytoplasmic 1 signaling pathway.
Results suggested that Formononetin acted as an antiresorption agent by blocking osteoclast activation.
Activated T lymphocytes suppress osteoclastogenesis by diverting early monocyte/macrophage progenitor lineage commitment towards dendritic cell differentiation through down‐regulation of receptor activator of nuclear factor‐kappaB and c‐Fos
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Transcriptional Program of Mouse Osteoclast Differentiation Governed by the Macrophage Colony-stimulating Factor and the Ligand for the Receptor Activator of NFκB*
Global gene expression suggests a more dynamic role of osteoclasts in bone physiology than previously anticipated and directs a three-stage differentiation program and induced genes for interaction with osteoblasts and immune and nerve cells.
Bifurcation of osteoclasts and dendritic cells from common progenitors.
Findings suggest that c-Fos is a key mediator of the lineage commitment between osteoclasts and dendritic cells and the lineage determination of osteoclast progenitors seen following GM-CSF treatment functions through the regulation of c- Fos expression.
Granulocyte-macrophage colony stimulating factor suppresses lipopolysaccharide-induced osteoclast-like cell formation in mouse bone marrow cultures.
LPS increased the amount of granulocyte-macrophage colony stimulating factor (GM-CSF) in the culture supernatant, and anti-GM- CSF antiserum almost abolished the inhibition of osteoclast formation by LPS, thereby indicating that GM-CSf generated by treatment with LPS may be responsible for the inhibitionof osteoc last formation.
Gene array identification of osteoclast genes: Differential inhibition of osteoclastogenesis by cyclosporin A and granulocyte macrophage colony stimulating factor
Time courses showed differential activation patterns of transcription factors with early induction of FUSE binding protein 1 (FBP) and c‐Jun, and later steady up regulation of NFATc1 and GABP by RANKL, implicating the upregulation of CSF2R in a possible feedback inhibition of osteoclastogenesis.
A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function.
Activation of NF-kB and c-Jun N-terminal kinase through the RANK-mediated signaling system appears to be involved in differentiation and activation of osteoclasts.
Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL.
  • H. Yasuda, N. Shima, T. Suda
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1998
A genetically engineered soluble form containing the extracellular domain of the protein induced OCL formation from spleen cells in the absence of osteoblasts/stromal cells, and it was concluded that the membrane-bound protein is osteoclast differentiation factor (ODF), a long-sought ligand mediating an essential signal to osteOClast progenitors for their differentiation into osteoclasts.
The Calcineurin/Nuclear Factor of Activated T Cells Signaling Pathway Regulates Osteoclastogenesis in RAW264.7 Cells*
Calcineurin is defined as an essential downstream effector of the RANKL-induced signal transduction pathway leading toward the induction of osteoclast differentiation and indicates that the activation of the NFATc1 transcription factor is sufficient to initiate a genetic program that results in the specification of the mature functional osteOClast cell phenotype.
CD1 molecule expression on human monocytes induced by granulocyte-macrophage colony-stimulating factor.
expression of CD1 molecules on monocytes complements the distribution of these structures on accessory cells, and their specific induction by GM-CSF strengthens the suggestion that CD1 is a family of crucial structures required for interaction between accessory cells and T cells.