Published online Apr 18, 2024. doi: 10.5312/wjo.v15.i4.363
Peer-review started: November 22, 2023
First decision: January 24, 2024
Revised: February 4, 2024
Accepted: March 19, 2024
Article in press: March 19, 2024
Published online: April 18, 2024
It is well known that exercise promotes bone growth and development. However, the underlying mechanisms by which exercise promotes bone formation are not fully understood.
Our previous findings suggest that the mechanosensitive lncRNA H19 is involved in the regulation of cartilage homeostasis. Therefore, we propose the hypothesis that mechanosensitive lncRNA H19 may be involved in mediating the process of exercise-promoted bone formation. This study will provide more theoretical basis for exercise promoting bone health.
The aim of this study was to investigate whether mechanosensitive lncRNA H19 could promote bone formation by targeting miR-149. This study reveals for the first time the potential regulatory role of the lncRNA H19/miR-149 axis in exercise-promoted bone formation, providing a scientific basis for the promotion of bone health by exercise.
The potential role of lncRNA H19/miR-149 axis in exercise-promoted bone formation was fully validated in vivo and in vitro by RT-qPCR, WB, IF, IHC, and micro-CT combined with bioinformatics analysis.
In vivo, exercise could activate autophagy by promoting the expression of lncRNA H19 and inhibiting the expression of miR-149, thereby promoting bone formation. In vitro, knockdown of lncRNA H19 was able to inhibit autophagy by upregulating miR-149 expression, thereby inhibiting osteogenic differentiation of bone mesenchymal stem cells.
Exercise can promote autophagy and bone formation through activation of the lncRNA H19/miR-149 axis.
The potential role of the lncRNA H19/miR-149/autophagy axis in exercise-promoted bone formation was further validated by gain of function and loss of function in animal experiments.