Swimming induces bone loss via regulating mechanical sensing pathways in bone marrow

ABSTRACT: Bone is an organ capable of perceiving external mechanical stress in real time and respond dynamically via mechanosensing proteins such as Piezo1 and YAP/TAZ. Upon sensing the mechano-signals, cells within the bone matrix collaborate to coordinate bone formation and resorption, while bone marrow cells are also stimulated and mobilized. High-load exercise stimulates osteoblast differentiation and bone formation. However, the mechanism through which the low-load exercises on bone homeostasis is still unclear. In this work, we established a long-term swimming training model to unload the mechanical stress in mice. Throughout the training model, we observed a significant loss in trabecular bone mass, as evidenced by microCT scanning and histological staining. Single-cell sequencing of the tibial bone marrow tissue revealed a significant increase in the percentage of bone marrow neutrophils, along with alterations in integrins and the ERK1/2 signaling pathway. Notably, the changes in both Integrins and the ERK1/2 signaling pathway in macrophages were more pronounced than in other cell types, which not only suggests a mechanical adaptive response in these cells. Moreover, the involvement of integrins is also critical for the crosstalk between monocyte precusors and macrophages during swimming. Together, this study provide a resource of the alterations of bone marrow cell gene expression profile during swimming and highlights the importance of Integrins and the ERK1/2 signaling pathway in the bone marrow microenvironment after swimming.

ORGANISM(S): Mus musculus

PROVIDER: GSE289853 | GEO | 2025/02/20

REPOSITORIES: GEO