最先端研究セミナー

Abstract：

Maintenance of bone throughout life requires continuous renewal of  osteoblasts.  Osteoblasts, originating from the perichondrium, accompany vascular invasion and lay down endochondral bone to replace cartilage.  Using a genetic recombination lineage tracing approach in mice, we previously  reported an additional source of osteoblasts,  that hypertrophic chondrocytes (HCs) can become osteogenic cells in fetal and postnatal endochondral bones and persist into adulthood. Moreover, the chondrocyte-to-osteoblast transition also occurs in bone repair. However, the signaling pathways that control the process and the molecular changes during the HC to osteoblast transition are  unknown. In my talk I will discuss how Wnt signaling controls fate determination  in the HC to osteoblast transition. I will also show how single cell transcriptomics can be used to dissect the lineage hierarchy during the fate transition from HC to osteoblast. The analyses reveal multiple molecular changes including cell cycle re-entry, during the lineage transition.

Reference:

L.Yang, K.Y. Tsang, H. C. Tang, D. Chan, K.S.E. Cheah (2014) Hypertrophic chondrocytes can become osteoblasts and osteocytes in endochondral bone formation. Proceedings of the National Academy of Sciences of the United States of America. 111: 12097–12102.

K.Y. Tsang, D. Chan, K.S.E. Cheah (2015). Fate of growth plate hypertrophic chondrocytes: Death or lineage extension? Development, Growth & Differentiation.  57: 179-192.

担当分野：　IRCMS　Guojun Sheng

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