Published online Jan 26, 2021. doi: 10.4252/wjsc.v13.i1.128
Peer-review started: September 1, 2020
First decision: September 15, 2020
Revised: November 1, 2020
Accepted: November 17, 2020
Article in press: November 17, 2020
Published online: January 26, 2021
Processing time: 142 Days and 0.1 Hours
Multipotent bone marrow stromal cells (BMSCs) form functional osteoblasts and are involved in bone formation. During aging, significant bone loss leads to osteoporosis and results in an increased risk of fracture.
We discovered that an early bone loss occurs as early as 1 mo in mice, and we would like to investigate the role of BMSCs during early bone loss.
To understand the functional alterations of BMSCs during the early bone loss and uncover the transcriptomic dynamics that underpin the early loss of osteogenic potential.
We collected BMSCs from mice at early to middle ages and assessed their self-renewal and differentiation potential. Subsequently, we obtained the transcriptomic profiles at a young age to reveal the features of BMSCs during early bone loss.
The colony-forming and osteogenic commitment capacity decreased at the age of 1 mo. At 3 mo, BMSCs were enriched in osteoblastic regulation genes, and at 7 mo, the transcriptomic features shifted toward adipogenic and DNA repair. The gene set enrichment analysis suggested the involvement of WNT and MAPK signaling pathways at the osteogenic phase and increased pro-inflammatory and apoptotic features at the latter phase.
We demonstrated the contribution of BMSCs to the early stage of age-related bone loss and uncovered the underlying transcriptomic dynamics.
Resolving the detailed cellular and molecular mechanism underlying bone aging is crucial. In this study, we demonstrated the role of BMSCs in early bone loss and revealed the transcriptomic dynamics to better understand the underlying molecular mechanism.