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Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment

Author

Listed:
  • Olaia Naveiras

    (Brigham and Women’s Hospital; Harvard Stem Cell Institute; Manton Center for Orphan Diseases; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
    Harvard Medical School)

  • Valentina Nardi

    (Brigham and Women’s Hospital; Harvard Stem Cell Institute; Manton Center for Orphan Diseases; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
    Harvard Medical School)

  • Pamela L. Wenzel

    (Brigham and Women’s Hospital; Harvard Stem Cell Institute; Manton Center for Orphan Diseases; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
    Harvard Medical School)

  • Peter V. Hauschka

    (Harvard Medical School and School of Dental Medicine, Boston, Massachusetts, 02115, USA)

  • Frederic Fahey

    (Children’s Hospital Boston, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA)

  • George Q. Daley

    (Brigham and Women’s Hospital; Harvard Stem Cell Institute; Manton Center for Orphan Diseases; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA
    Harvard Medical School)

Abstract

Bad blood from fat cells Adult bone marrow contains numerous adipocytes, whose numbers correlate inversely with the haematopoietic activity. Disorders of excess haematopoiesis, such as pernicious anaemia and leukaemia, are typically accompanied by haematopoietic infiltration of the fatty marrow of the long bones. It has been unclear whether adipocytes participate in haematopoietic regulation or simply expand to fill marrow space. The answer appears to be that far from making up the numbers, fat cells play a critical physiological role in the bone marrow microenvironment. Experiments in mice show that adipocyte-rich marrow contains fewer blood-forming stem cells and progenitors than adipocyte-poor marrow. Genetically 'fat-free' mice and mice treated with a drug that blocks adipocyte production generated new blood cells more quickly than wild-type animals after a bone-marrow transplant, suggesting that blocking marrow adipogenesis may enhance haematopoietic recovery in clinical bone-marrow transplantation.

Suggested Citation

  • Olaia Naveiras & Valentina Nardi & Pamela L. Wenzel & Peter V. Hauschka & Frederic Fahey & George Q. Daley, 2009. "Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment," Nature, Nature, vol. 460(7252), pages 259-263, July.
    • Handle: RePEc:nat:nature:v:460:y:2009:i:7252:d:10.1038_nature08099
    DOI: 10.1038/nature08099
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    Cited by:

    1. Tongling Huang & Zhaocheng Lu & Zihui Wang & Lixin Cheng & Lu Gao & Jun Gao & Ning Zhang & Chang-An Geng & Xiaoli Zhao & Huaiyu Wang & Chi-Wai Wong & Kelvin W. K. Yeung & Haobo Pan & William Weijia Lu, 2024. "Targeting adipocyte ESRRA promotes osteogenesis and vascular formation in adipocyte-rich bone marrow," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    2. Trent D. Hall & Hyunjin Kim & Mahmoud Dabbah & Jacquelyn A. Myers & Jeremy Chase Crawford & Antonio Morales-Hernandez & Claire E. Caprio & Pramika Sriram & Emilia Kooienga & Marta Derecka & Esther A. , 2022. "Murine fetal bone marrow does not support functional hematopoietic stem and progenitor cells until birth," Nature Communications, Nature, vol. 13(1), pages 1-18, December.
    3. Kei Kohno & Hiroto Narimatsu & Yosuke Shiono & Ikuko Suzuki & Yuichi Kato & Ri Sho & Katsumi Otani & Kenichi Ishizawa & Hidetoshi Yamashita & Isao Kubota & Yoshiyuki Ueno & Takeo Kato & Akira Fukao & , 2016. "High Serum Adiponectin Level Is a Risk Factor for Anemia in Japanese Men: A Prospective Observational Study of 1,029 Japanese Subjects," PLOS ONE, Public Library of Science, vol. 11(12), pages 1-14, December.
    4. N. Zioni & A. Akhiad Bercovich & N. Chapal-Ilani & Tal Bacharach & N. Rappoport & A. Solomon & R. Avraham & E. Kopitman & Z. Porat & M. Sacma & G. Hartmut & M. Scheller & C. Muller-Tidow & D. Lipka & , 2023. "Inflammatory signals from fatty bone marrow support DNMT3A driven clonal hematopoiesis," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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