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TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone

Author

Listed:
  • Hiroaki Saito

    (University Medical Center Hamburg-Eppendorf)

  • Andreas Gasser

    (University Medical Center Hamburg-Eppendorf)

  • Simona Bolamperti

    (University Medical Center Hamburg-Eppendorf)

  • Miki Maeda

    (University Medical Center Hamburg-Eppendorf)

  • Levi Matthies

    (University Medical Center Hamburg-Eppendorf)

  • Katharina Jähn

    (University Medical Center Hamburg-Eppendorf)

  • Courtney L. Long

    (University Medical Center Hamburg-Eppendorf)

  • Hartmut Schlüter

    (University Medical Center Hamburg-Eppendorf)

  • Marcel Kwiatkowski

    (University Medical Center Hamburg-Eppendorf)

  • Vaibhav Saini

    (Massachusetts General Hospital)

  • Paola Divieti Pajevic

    (Massachusetts General Hospital
    School of Dental Medicine)

  • Teresita Bellido

    (Indiana University School of Medicine)

  • Andre J. Wijnen

    (Mayo Clinic)

  • Khalid S. Mohammad

    (Indiana School of Medicine)

  • Theresa A. Guise

    (Indiana School of Medicine)

  • Hanna Taipaleenmäki

    (University Medical Center Hamburg-Eppendorf)

  • Eric Hesse

    (University Medical Center Hamburg-Eppendorf
    Indiana University School of Medicine)

Abstract

Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.

Suggested Citation

  • Hiroaki Saito & Andreas Gasser & Simona Bolamperti & Miki Maeda & Levi Matthies & Katharina Jähn & Courtney L. Long & Hartmut Schlüter & Marcel Kwiatkowski & Vaibhav Saini & Paola Divieti Pajevic & Te, 2019. "TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08778-x
    DOI: 10.1038/s41467-019-08778-x
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