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

Author

Listed:
  • Masaru Ishii

    (Lymphocyte Biology Section
    Laboratory of Biological Imaging, WPI-Immunology Frontier Research Center, Osaka University
    National Osaka Minami Medical Center)

  • 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
    Program in Systems Immunology and Infectious Disease Modeling, National Institute of Allergy and Infectious Diseases, and,)

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.

Suggested Citation

  • Masaru Ishii & Jackson G. Egen & Frederick Klauschen & Martin Meier-Schellersheim & Yukihiko Saeki & Jean Vacher & Richard L. Proia & Ronald N. Germain, 2009. "Sphingosine-1-phosphate mobilizes osteoclast precursors and regulates bone homeostasis," Nature, Nature, vol. 458(7237), pages 524-528, March.
    • Handle: RePEc:nat:nature:v:458:y:2009:i:7237:d:10.1038_nature07713
    DOI: 10.1038/nature07713
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    Cited by:

    1. Maki Uenaka & Erika Yamashita & Junichi Kikuta & Akito Morimoto & Tomoka Ao & Hiroki Mizuno & Masayuki Furuya & Tetsuo Hasegawa & Hiroyuki Tsukazaki & Takao Sudo & Keizo Nishikawa & Daisuke Okuzaki & , 2022. "Osteoblast-derived vesicles induce a switch from bone-formation to bone-resorption in vivo," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. João Pedro Pereira & Jason G Cyster & Ying Xu, 2010. "A Role for S1P and S1P1 in Immature-B Cell Egress from Mouse Bone Marrow," PLOS ONE, Public Library of Science, vol. 5(2), pages 1-6, February.
    3. Shin Koyama & Eijiro Narita & Naoki Shinohara & Junji Miyakoshi, 2014. "Effect of an Intermediate-Frequency Magnetic Field of 23 kHz at 2 mT on Chemotaxis and Phagocytosis in Neutrophil-Like Differentiated Human HL-60 Cells," IJERPH, MDPI, vol. 11(9), pages 1-11, September.

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