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TNF‑α and RANKL promote osteoclastogenesis by upregulating RANK via the NF‑κB pathway.

Gang Luo1, Fangfei Li1, Xiaoming Li1

  • 1State Key Laboratory of Trauma, Burns and Combined Injury, Department 4, Research Institute of Field Surgery, Third Military Medical University, Chongqing 400042, P.R. China.

Molecular Medicine Reports
|March 8, 2018
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor alpha (TNF‑α) combined with RANKL significantly enhances osteoclast differentiation. The nuclear factor kappa B (NF‑κB) pathway is crucial for this TNF‑α-induced osteoclastogenesis.

Keywords:
tumor necrosis factor αreceptor activator of nuclear factor-κBosteoclastnuclear factor-κB

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Area of Science:

  • Immunology
  • Cell Biology
  • Bone Biology

Background:

  • Tumor necrosis factor alpha (TNF‑α) is implicated in inflammatory osteolysis.
  • The precise mechanisms of TNF‑α in osteoclast recruitment and differentiation are not fully understood.

Purpose of the Study:

  • To elucidate the role of TNF‑α in osteoclast differentiation.
  • To investigate the involvement of the nuclear factor kappa B (NF‑κB) pathway in TNF‑α-mediated osteoclastogenesis.

Main Methods:

  • Mouse bone marrow-derived macrophages (BMMs) were used as osteoclast precursors.
  • Osteoclastogenesis was induced using macrophage colony-stimulating factor and receptor activator of nuclear factor (NF)‑κB ligand (RANKL), with or without TNF‑α.
  • The NF‑κB pathway was inhibited using BAY 11‑7082.

Main Results:

  • TNF‑α alone did not induce osteoclastogenesis.
  • TNF‑α in combination with RANKL significantly stimulated osteoclast differentiation and upregulated osteoclast marker genes.
  • NF‑κB inhibition prevented mature osteoclast formation and the upregulation of osteoclast markers.

Conclusions:

  • TNF‑α cooperates with RANKL to induce osteoclast differentiation.
  • The NF‑κB pathway plays a critical role in TNF‑α-mediated osteoclastogenesis.
  • These findings offer insights into the mechanisms of inflammatory osteolysis.