IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms12794.html
   My bibliography  Save this article

GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation

Author

Listed:
  • Weiqing Liu

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Liyan Zhou

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Chenchen Zhou

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Shiwen Zhang

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Junjun Jing

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Liang Xie

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Ningyuan Sun

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Xiaobo Duan

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Wei Jing

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Xing Liang

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Hu Zhao

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Ling Ye

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Qianming Chen

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

  • Quan Yuan

    (State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University)

Abstract

Osteoporosis is an age-related disease that affects millions of people. Growth differentiation factor 11 (GDF11) is a secreted member of the transforming growth factor beta (TGF-β) superfamily. Deletion of Gdf11 has been shown to result in a skeletal anterior–posterior patterning disorder. Here we show a role for GDF11 in bone remodelling. GDF11 treatment leads to bone loss in both young and aged mice. GDF11 inhibits osteoblast differentiation and also stimulates RANKL-induced osteoclastogenesis through Smad2/3 and c-Fos-dependent induction of Nfatc1. Injection of GDF11 impairs bone regeneration in mice and blocking GDF11 function prevents oestrogen-deficiency-induced bone loss and ameliorates age-related osteoporosis. Our data demonstrate that GDF11 is a previously unrecognized regulator of bone remodelling and suggest that GDF11 is a potential target for treatment of osteoporosis.

Suggested Citation

  • Weiqing Liu & Liyan Zhou & Chenchen Zhou & Shiwen Zhang & Junjun Jing & Liang Xie & Ningyuan Sun & Xiaobo Duan & Wei Jing & Xing Liang & Hu Zhao & Ling Ye & Qianming Chen & Quan Yuan, 2016. "GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation," Nature Communications, Nature, vol. 7(1), pages 1-13, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12794
    DOI: 10.1038/ncomms12794
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms12794
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms12794?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12794. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.