Bone marrow mesenchymal stem cells and TGF-β signaling in bone remodeling.
During bone resorption, abundant factors previously buried in the bone matrix are released into the bone marrow microenvironment, which results in recruitment and differentiation of bone marrow mesenchymal stem cells (MSCs) for subsequent bone formation, temporally and spatially coupling bone remodeling. Parathyroid hormone (PTH) orchestrates the signaling of many pathways that direct MSC fate. The spatiotemporal release and activation of matrix TGF-β during osteoclast bone resorption recruits MSCs to bone-resorptive sites. Dysregulation of TGF-β alters MSC fate, uncoupling bone remodeling and causing skeletal disorders. Modulation of TGF-β or PTH signaling may reestablish coupled bone remodeling and be a potential therapy.
Janet L
JL
Crane
Xu
X
Cao
D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology*; D001859:Bone Neoplasms / Q000378:metabolism; D016723:Bone Remodeling; D001862:Bone Resorption; D002454:Cell Differentiation; D019070:Cell Lineage; D005786:Gene Expression Regulation; D006706:Homeostasis; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000166:cytology*; D010003:Osteoarthritis / Q000378:metabolism; D010010:Osteoclasts; D010012:Osteogenesis; D010281:Parathyroid Hormone / Q000378:metabolism*; D015398:Signal Transduction; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000378:metabolism*
D010281:Parathyroid Hormone; D016212:Transforming Growth Factor beta