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Growth plate-derived hedgehog-signal-responsive cells provide skeletal tissue components in growing bone

Authors
  • Haraguchi, Ryuma1
  • Kitazawa, Riko1, 2
  • Imai, Yuuki3
  • Kitazawa, Sohei1
  • 1 Ehime University Graduate School of Medicine, Department of Molecular Pathology, Shitsukawa, Toon City, Ehime, 791-0295, Japan , Toon City (Japan)
  • 2 Ehime University Hospital, Department of Diagnostic Pathology, Shitsukawa, Toon City, Ehime, 791-0295, Japan , Toon City (Japan)
  • 3 Ehime University Graduate School of Medicine, Division of Integrative Pathophysiology, Proteo-Science Center, Shitsukawa, Toon City, Ehime, 791-0295, Japan , Toon City (Japan)
Type
Published Article
Journal
Histochemistry and Cell Biology
Publisher
Springer Berlin Heidelberg
Publication Date
Jan 22, 2018
Volume
149
Issue
4
Pages
365–373
Identifiers
DOI: 10.1007/s00418-018-1641-5
Source
Springer Nature
Keywords
License
Yellow

Abstract

Longitudinal bone growth progresses by continuous bone replacement of epiphyseal cartilaginous tissue, known as “growth plate”, produced by columnar proliferated- and differentiated-epiphyseal chondrocytes. The endochondral ossification process at the growth plate is governed by paracrine signals secreted from terminally differentiated chondrocytes (hypertrophic chondrocytes), and hedgehog signaling is one of the best known regulatory signaling pathways in this process. Here, to investigate the developmental relationship between longitudinal endochondral bone formation and osteogenic progenitors under the influence of hedgehog signaling at the growth plate, genetic lineage tracing was carried out with the use of Gli1CreERT2 mice line to follow the fate of hedgehog-signal-responsive cells during endochondral bone formation. Gli1CreERT2 genetically labeled cells are detected in hypertrophic chondrocytes and osteo-progenitors at the chondro-osseous junction (COJ); these progeny then commit to the osteogenic lineage in periosteum, trabecular and cortical bone along the developing longitudinal axis. Furthermore, in ageing bone, where longitudinal bone growth ceases, hedgehog-signal responsiveness and its implication in osteogenic lineage commitment is significantly weakened. These results show, for the first time, evidence of the developmental contribution of endochondral progenitors under the influence of epiphyseal chondrocyte-derived secretory signals in longitudinally growing bone. This study provides a precise outline for assessing the skeletal lineage commitment of osteo-progenitors in response to growth-plate-derived regulatory signals during endochondral bone formation.

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