Cheng YH, Liu SF, Dong JC, Bian Q. Transcriptomic alterations underline aging of osteogenic bone marrow stromal cells. World J Stem Cells 2021; 13(1): 128-138 [PMID: 33584984 DOI: 10.4252/wjsc.v13.i1.128]
Corresponding Author of This Article
Qin Bian, MD, PhD, Professor, Department of Integrative Medicine, Huashan Hospital, Fudan University, Middle Wulumuqi Road, Shanghai 200040, China. bianqin213@126.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Yu-Hao Cheng, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States
Shu-Fen Liu, Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai 200030, China
Jing-Cheng Dong, Qin Bian, Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China
Author contributions: Liu SF and Bian Q performed the in vivo and ex vivo experiments, respectively; Cheng YH wrote the manuscript and analyzed the data; Dong JC and Bian Q edited the manuscript and provided feedback; Bian Q designed the project.
Supported bythe National Natural Science Foundation of China, No. 81573992.
Institutional animal care and use committee statement: The study was approved by the Shanghai Animal Ethics Committee.
Conflict-of-interest statement: Qin Bian is currently a research associate at Johns Hopkins University. The work has been done prior to her entrance to Johns Hopkins University.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Qin Bian, MD, PhD, Professor, Department of Integrative Medicine, Huashan Hospital, Fudan University, Middle Wulumuqi Road, Shanghai 200040, China. bianqin213@126.com
Received: September 1, 2020 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
ARTICLE HIGHLIGHTS
Research background
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.
Research motivation
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.
Research objectives
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.
Research methods
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.
Research results
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.
Research conclusions
We demonstrated the contribution of BMSCs to the early stage of age-related bone loss and uncovered the underlying transcriptomic dynamics.
Research perspectives
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.
