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Beta2-microglobulin stimulates osteoclast formation.

C Menaa1, E Esser, S M Sprague

  • 1Evanston Northwestern Healthcare and Northwestern University Feinberg School of Medicine, Evanston, Illinois 60201, USA.

Kidney International
|March 28, 2008
PubMed
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Beta-2 microglobulin (beta(2)M) directly stimulates osteoclast activity, causing bone destruction in dialysis-related amyloidosis. This process involves cytokine production and is linked to chronic kidney disease complications.

Area of Science:

  • Nephrology
  • Bone Biology
  • Immunology

Background:

  • Dialysis-related amyloidosis (DRA) is a complication of long-term chronic kidney disease (CKD).
  • DRA involves beta-2 microglobulin (beta(2)M) amyloid deposition in osteoarticular tissues, leading to arthropathy, bone cysts, and fractures.
  • Osteolytic lesions are characteristic findings in DRA.

Purpose of the Study:

  • To investigate if beta(2)M directly stimulates osteoclast activity.
  • To determine if local cytokine production mediates beta(2)M-induced bone destruction.
  • To elucidate the role of beta(2)M in the pathogenesis of bone complications in CKD.

Main Methods:

  • Cultured mouse marrow cells, colony-forming unit granulocyte macrophages, and RAW 264.7 monocytic cells were treated with beta(2)M.

Related Experiment Videos

  • Osteoclastogenesis was assessed by counting tartrate-resistant alkaline phosphatase-positive multinucleated cells.
  • Cytokine expression (TNF-alpha, IL-1) was measured, and the effect of a TNF-alpha-neutralizing antibody was evaluated.

    • Main Results:

    • Beta-2 microglobulin (beta(2)M) induced a dose-dependent increase in osteoclast formation.
    • Osteoclastogenesis occurred independently of osteoblasts or stromal cells.
    • Beta(2)M upregulated TNF-alpha and IL-1 expression, and TNF-alpha neutralization blocked beta(2)M-induced osteoclast formation.

    Conclusions:

    • Beta-2 microglobulin (beta(2)M) directly stimulates osteoclastogenesis.
    • Tumor necrosis factor-alpha (TNF-alpha) mediates the osteoclastogenic effect of beta(2)M.
    • These findings support a direct role for beta(2)M in causing bone destruction in dialysis-related amyloidosis and CKD.