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Bone sialoprotein deficiency impairs osteoclastogenesis and mineral resorption in vitro. | LitMetric

AI Article Synopsis

  • Bone sialoprotein (BSP) and osteopontin (OPN) are proteins that interact with bone cells and influence bone mineralization, and BSP knockout mice (BSP(-/-)) exhibit higher bone mass but lower bone formation activity compared to normal mice (BSP(+/+)).
  • In cultures, BSP(-/-) preosteoclasts show significantly reduced cell numbers, impaired proliferation, and increased cell death, but adding RGD-containing proteins can restore their numbers to that of normal cells.
  • BSP(-/-) osteoclasts also express altered levels of certain genes related to cell adhesion and bone resorption, indicating that while they struggle with osteoclast formation and mineral resorption, there's some functional

Article Abstract

Bone sialoprotein (BSP) and osteopontin (OPN) belong to the small integrin-binding ligand N-linked glycoprotein (SIBLING) family, whose members interact with bone cells and bone mineral. Previously, we showed that BSP knockout (BSP(-/-) ) mice have a higher bone mass than wild type (BSP(+/+) ) littermates, with very low bone-formation activity and reduced osteoclast surfaces and numbers. Here we report that approximately twofold fewer tartrate-resistant acid phosphatase (TRACP)-positive cells and approximately fourfold fewer osteoclasts form in BSP(-/-) compared with BSP(+/+) spleen cell cultures. BSP(-/-) preosteoclast cultures display impaired proliferation and enhanced apoptosis. Addition of RGD-containing proteins restores osteoclast number in BSP(-/-) cultures to BSP(+/+) levels. The expression of osteoclast-associated genes is markedly altered in BSP(-/-) osteoclasts, with reduced expression of cell adhesion and migration genes (αV integrin chain and OPN) and increased expression of resorptive enzymes (TRACP and cathepsin K). The migration of preosteoclasts and mature osteoclasts is impaired in the absence of BSP, but resorption pit assays on dentine slices show no significant difference in pit numbers between BSP(+/+) and BSP(-/-) osteoclasts. However, resorption of mineral-coated slides by BSP(-/-) osteoclasts is markedly impaired but is fully restored by coating the mineral substrate with hrBSP and partly restored by hrOPN coating. In conclusion, lack of BSP affects both osteoclast formation and activity, which is in accordance with in vivo findings. Our results also suggest at least some functional redundancy between BSP and OPN that remains to be clarified.

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http://dx.doi.org/10.1002/jbmr.245DOI Listing

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