November 29, 2022
A research group led by Associate Professor Yuki Matsushita of the Graduate School of Biomedical Sciences , Nagasaki University and Dr. Noriaki Ono of the University of Texas has discovered an important mechanism involved in bone development and growth through international joint research at three universities including the University of Michigan, USA.
In endochondral bone development, bone-forming osteoblasts and bone marrow stromal cells have dual origins in the fetal cartilage and its surrounding perichondrium. However, how early perichondrial cells distinctively contribute to developing bones remain unidentified. Here we show using in vivo cell-lineage analyses that Dlx5+ fetal perichondrial cells marked by Dlx5-creER do not generate cartilage but sustainably contribute to cortical bone and marrow stromal compartments in a manner complementary to fetal chondrocyte derivatives under the regulation of Hedgehog signaling. Postnatally, Dlx5+ fetal perichondrial cell derivatives preferentially populate the diaphyseal marrow stroma with a dormant adipocyte-biased state and are refractory to parathyroid hormone-induced bone anabolism. Therefore, early perichondrial cells of the fetal cartilage are destined to become an adipogenic subset of stromal cells in postnatal diaphyseal bone marrow, supporting the theory that the adult bone marrow stromal compartments are developmentally prescribed within the two distinct cells-of-origins of the fetal bone anlage.
Title：The fate of early perichondrial cells in developing bone
Author information：Yuki Matsushita1,2, Angel Ka Yan Chu3, Chiaki Tsutsumi-Arai1,
Shion Orikasa1, Mizuki Nagata1, Sunny Y. Wong4, Joshua D. Welch3, Wanida Ono1,
1.University of Texas Health Science Center at Houston School of Dentistry
2.Department of Cell Biology, Nagasaki University Graduate School of Biomedical Sciences
3.Department of Computational Medicine and Bioinformatics, University of Michigan
4.Department of Dermatology, University of Michigan Medical School, Ann Arbor MI 48109
* Corresponding author
Journal：Nature Communications 13,7319 (2022)
▶This release is also available in Japanese.