Smad4 is required for maintaining normal murine postnatal bone homeostasis

DOI PDF 被引用文献1件
  • Xiaohong Tan
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Tujun Weng
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Jishuai Zhang
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Jian Wang
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Wenlong Li
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Haifeng Wan
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Yu Lan
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Xuan Cheng
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Ning Hou
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Haihong Liu
    Laboratory of Analytical Microbiology, Institute of Microbiology and Epidemiology, Beijing 100071, P.R. China
  • Jun Ding
    Model Animal Research Center, Nanjing University, P.R. China
  • Fuyu Lin
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China
  • Ruifu Yang
    Laboratory of Analytical Microbiology, Institute of Microbiology and Epidemiology, Beijing 100071, P.R. China
  • Xiang Gao
    Model Animal Research Center, Nanjing University, P.R. China
  • Di Chen
    Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA
  • Xiao Yang
    Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China

書誌事項

公開日
2007-07-01
DOI
  • 10.1242/jcs.03466
公開者
The Company of Biologists

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説明

<jats:p>Transforming growth factor β (TGFβ) is a multifunctional cytokine involved in skeletal development. Smad4 is the central intracellular mediator of TGFβ signaling. Our previous studies reveal that Smad4 is required for maintaining the normal development of chondrocytes in the growth plate. However, its biological function during postnatal bone remodeling is largely unknown. To investigate the role of Smad4 in maintaining bone homeostasis, we disrupted the Smad4 gene in differentiated osteoblasts using the Cre-loxP system. The Smad4 mutant mice exhibited lower bone mass up to 6 months of age. The proliferation and function of the mutant osteoblasts were significantly decreased. Bone mineral density, bone volume, bone formation rate and osteoblast numbers were remarkably reduced in Smad4 mutants. Intriguingly, the trabecular bone volume in Smad4 mutant mice older than 7 months was higher than that of controls whereas the calvarial and cortical bone remained thinner than in controls. This correlated with reduced bone resorption possibly caused by downregulation of TGFβ1 and alteration of the ligand receptor activator of NF-κB (RANKL)-osteoprotegerin (OPG) axis. These studies demonstrate essential roles of Smad4-mediated TGFβ signaling in coupling bone formation and bone resorption and maintaining normal postnatal bone homeostasis.</jats:p>

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