Elucidation of the new bone homeostasis maintained by gravitational loading – Publicly Invited Research 2018－2019

  1. A01 Ogura
  2. A01 H. Takahashi
  3. A01 S. Takahashi
  4. A01 Michiue
  5. A01 Hinoi
  6. A01 Tsumoto
  7. A01 Nikawa
  8. A01 Chatani
  9. A01 Kawakami
  10. A01 Akiyama
  11. A01 Tomita
  1. A02 Shinohara
  2. A02 Mieda
  3. A02 Maekawa
  4. A02 Abe
  5. A02 Ohgami
  6. A02 Kawano
  7. A02 Takano
  1. A03 Suzuki
  2. A03 Nakamura
  3. A03 Harada
  4. A03 Kobayashi
  5. A03 Miyamoto
  6. A03 Funayama
  7. A03 Kakinuma
  1. B01 Lazarus
  2. B01 Kato
  3. B01 Kunieda
  4. B01 Kitaya
  5. B01 Sawano
Research Subject Elucidation of the new bone homeostasis maintained by gravitational loading
Research Group Leader
name
Haruko Takano
Senior Researcher, Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute
Website
http://www.ncvc.go.jp/english/res/str_ana/
Research Collaborator(s)
  • Ayano Chiba
    Senior Researcher, Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute

Exposure to microgravity leads to compromised bone homeostasis, which results in acute and severe bone loss. To maintain bone mass, skeletal stem cells (SSCs) give rise to bone forming osteoblasts continuously. However, under the microgravity environment, osteocyte-derived signals induce bone resorption through activation of osteoclasts and inhibit the differentiation of SSCs into osteoblasts. It has been well-known that cosmonauts exhibit pronounced bone loss preferentially in weight-bearing bones when exposed to microgravity, suggesting the existence of weight sensing mechanism for maintaining bone homeostasis.

Osteocrin (OSTN) is a secretory protein that belongs to the natriuretic peptide (NP) hormone family. We previously found that OSTN expression is enriched in the weight-bearing regions of the bones and downregulated by neurectomy-induced unloading. Our studies also suggested that OSTN might enhance the specification and differentiation of SSCs into osteoblast lineage. Considering these findings, we hypothesize that OSTN might be a key mediator involved in regulation of loading-induced bone formation. Thus, to address this hypothesis, we will analyze (1) OSTN regulates loading-induced bone formation by promoting osteoblast differentiation and (2) OSTN inhibits bone loss in microgravity.