Sphingosine-1-phosphate mobilizes osteoclast precursors and regulates bone homeostasis

Masaru Ishii, Jackson G. Egen, Frederick Klauschen, Martin Meier-Schellersheim, Yukihiko Saeki, Jean Vacher, Richard L. Proia and Ronald N. Germain ()
Additional contact information
Masaru Ishii: Lymphocyte Biology Section
Jackson G. Egen: Lymphocyte Biology Section
Frederick Klauschen: Program in Systems Immunology and Infectious Disease Modeling, National Institute of Allergy and Infectious Diseases, and,
Martin Meier-Schellersheim: Program in Systems Immunology and Infectious Disease Modeling, National Institute of Allergy and Infectious Diseases, and,
Yukihiko Saeki: National Osaka Minami Medical Center
Jean Vacher: Institut de Recherches Cliniques de Montréal
Richard L. Proia: Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-1892, USA
Ronald N. Germain: Lymphocyte Biology Section

Nature, 2009, vol. 458, issue 7237, 524-528

Abstract: Controlling bone resorption Bone is a dynamic tissue, constantly undergoing growth, remodelling and degradation. Central to these processes are the osteoclasts, bone-resorbing multinuclear giant cells that differentiate from mononuclear macrophage/monocyte-lineage haematopoietic precursors. Normally bone resorption is balanced by the activity of bone-forming osteoblasts, but in bone-destructive disorders such as osteoporosis, osteoclast activity outpaces osteoblast activity. Now using a mouse model of hormone-deprivation osteoporosis, the blood-born lipid mediator sphingosine-1-phosphate is identified as a key mediator of bone demineralization. It controls the migratory behaviour of osteoclast precursors, thereby regulating bone homeostasis. As a pivotal control point in osteoclastogenesis, sphingosine-1-phosphate may have potential, as a therapeutic target in bone-resorptive disorders.

Date: 2009
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DOI: 10.1038/nature07713

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