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Related Experiment Video

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Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
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S100A12 facilitates osteoclast differentiation from human monocytes.

Miwa Nishida1,2, Jun Saegusa1,3, Shino Tanaka1

  • 1Department of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan.

Plos One
|September 21, 2018
PubMed
Summary

S100A12 promotes osteoclast formation and bone resorption, contributing to inflammatory osteolysis. Blocking RAGE and TLR4 pathways negates these effects, suggesting S100A12 as a therapeutic target for bone inflammation.

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Area of Science:

  • Biochemistry
  • Immunology
  • Bone Biology

Background:

  • Osteoclasts are crucial for bone homeostasis and inflammatory osteolysis.
  • Inflammatory cytokines like IL-1, IL-6, and TNF-α influence osteoclast activity, but their precise roles are unclear.
  • S100A12, a pro-inflammatory protein, has unknown effects on osteoclast differentiation.

Purpose of the Study:

  • To investigate the direct effects of S100A12 on human osteoclast formation and function in vitro.
  • To elucidate the role of S100A12 in inflammatory osteolysis.

Main Methods:

  • Human osteoclasts were cultured in vitro with S100A12 and RANKL.
  • Osteoclast formation, morphology, and expression of key osteoclast markers (NFATc1, ACP5, CALCR, ITGβ3, CTSK, CA2) were assessed.
  • The impact of blocking RAGE and TLR4 pathways on S100A12 effects was evaluated.

Main Results:

  • S100A12 significantly facilitated osteoclast formation and enhanced bone resorption.
  • Elevated expression of osteoclast-related molecules was observed with S100A12 treatment.
  • Blocking RAGE and TLR4 pathways abrogated the pro-osteoclastogenic effects of S100A12.

Conclusions:

  • S100A12 directly promotes human osteoclast differentiation and bone resorption.
  • S100A12 mediates its effects through RAGE and TLR4 signaling pathways.
  • S100A12 represents a potential therapeutic target for managing inflammatory osteolysis.