MCP-1 expressed by osteoclasts stimulates osteoclastogenesis in an autocrine/paracrine manner

Kana Miyamoto, Ken Ninomiya, Koh Hei Sonoda, Yoshiteru Miyauchi, Hiroko Hoshi, Ryotaro Iwasaki, Hiroya Miyamoto, Shigeyuki Yoshida, Yuiko Sato, Hideo Morioka, Kazuhiro Chiba, Kensuke Egashira, Toshio Suda, Yoshiaki Toyama, Takeshi Miyamoto

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76 Citations (Scopus)


Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that plays a critical role in the recruitment and activation of leukocytes. Here, we describe that multinuclear osteoclast formation was significantly inhibited in cells derived from MCP-1-deficient mice. MCP-1 has been implicated in the regulation of osteoclast cell-cell fusion; however defects of multinuclear osteoclast formation in the cells from mice deficient in DC-STAMP, a seven transmembrane receptor essential for osteoclast cell-cell fusion, was not rescued by recombinant MCP-1. The lack of MCP-1 in osteoclasts resulted in a down-regulation of DC-STAMP, NFATc1, and cathepsin K, all of which were highly expressed in normal osteoclasts, suggesting that osteoclast differentiation was inhibited in MCP-1-deficient cells. MCP-1 alone did not induce osteoclastogenesis, however, the inhibition of osteoclastogenesis in MCP-1-deficient cells was restored by addition of recombinant MCP-1, indicating that osteoclastogenesis was regulated in an autocrine/paracrine manner by MCP-1 under the stimulation of RANKL in osteoclasts.

Original languageEnglish
Pages (from-to)373-377
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Jun 5 2009

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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