Bone cell interactions through Eph/ephrin: Bone modeling, remodeling and associated diseases

Koichi Matsuo, Natsuko Otaki

Research output: Contribution to journalReview article

87 Citations (Scopus)

Abstract

Bones cannot properly form or be maintained without cell-cell interactions through ephrin ligands and Eph receptors. Cell culture analysis and evaluation of genetic mouse models and human diseases reveal various ephrins and Eph functions in the skeletal system. Migration, attachment and spreading of mesenchymal stem cells are regulated by ephrinB ligands and EphB receptors. ephrinB1 loss-of-function is associated with craniofrontonasal syndrome (CFN S) in humans and mice. In bone remodeling, ephrinB2 is postulated to act as a "coupling stimulator." In that case, bidirectional signaling between osteoclastic ephrinB2 and osteoblastic EphB4 suppresses osteoclastic bone resorption and enhances osteoblastic bone formation, facilitating the transition between these two states. Parathyroid hormone (PTH) induces ephrinB2 in osteoblasts and enhances osteoblastic bone formation. In contrast to ephrinB2, ephrinA2 acts as a "coupling inhibitor," since ephrinA2 reverse signaling into osteoclasts enhances osteoclastogenesis and EphA2 forward signaling into osteoblasts suppresses osteoblastic bone formation and mineralization. Furthermore, ephrins and Ephs likely modulate pathological conditions such as osteoarthritis, rheumatoid arthritis, multiple myeloma and osteosarcoma. This review focuses on ephrin/Eph-mediated cell-cell interactions in bone biology.

Original languageEnglish
Pages (from-to)148-156
Number of pages9
JournalCell Adhesion and Migration
Volume6
Issue number2
DOIs
Publication statusPublished - 2012

Keywords

  • Cell-cell interaction
  • Chondrocyte
  • Coupling factor
  • Coupling inhibitor
  • Multiple myeloma
  • Osteoarthritis
  • Osteoblast
  • Osteoclast
  • Osteosarcoma
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

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