Mechanisms underlying bone loss during spaceflight ~Elucidation of the regulatory mechanism for expression of an osteoclast differentiation factor, RANKL – Publicly Invited Research

  1. A01 Akiyama
  2. A01 Ochi
  3. A01 Chatani
  4. A01 Seiki
  5. A01 Nikawa
  6. A01 Kawakami
  7. A01 Tomita
  8. A01 Honda
  1. A02 Shinohara
  2. A02 Maekawa
  3. A02 Ohgami
  4. A02 Nishimura
  5. A02 Kawano
  6. A02 Iwase
  7. A02 Furuichi
  8. A02 Myung
  9. A02 Kitamura
  1. A03 Nakamura
  2. A03 Harada
  3. A03 Ide
  4. A03 Shirai
  5. A03 Kakinuma
  1. B01 Lazarus
  2. B01 Miwa
  3. B01 Kunieda
  4. B01 Shimada
  5. B01 Kitaya
  6. B01 Sawano
Research Subject Mechanisms underlying bone loss during spaceflight ~Elucidation of the regulatory mechanism for expression of an osteoclast differentiation factor, RANKL
Research Group Leader
Masahiro Shinohara
  • Masahiro Shinohara
    Junior Associate Professor, Department of Systems BioMedicine, Tokyo Medical and Dental University
    Website
    http://
Research Collaborator(s)
  • Hironobu Morita
    Professor, School of Medicine, Gifu University
  • Satoru Takahashi
    Professor, School of Medicine and Medical Sciences, University of Tsukuba
  • Dai Shiba
    Associate Senior Engineer, JAXA

Mechanical loading is a critical factor for maintaining bone tissue homeostasis. Bone-forming osteoblasts and bone-resorbing osteoclasts have critical roles in bone homeostasis. Under mechanical unloading conditions such as microgravity, both bone mass and strength decrease due to enhanced osteoclastic bone resorption, leading to osteoporosis, a bone disease with a high risk of bone fracture. RANKL is a cytokine that plays an essential role in the differentiation of osteoclasts. RANKL is known to be expressed by osteoblasts/osteocytes under physiological conditions, and by T cells, B cells or synovial fibroblasts under certain pathological conditions. However, cells expressing RANKL under mechanical unloading conditions are largely unknown.
In this study, we therefore identify the cells expressing RANKL by using RANKL reporter transgenic mice and also analyze the molecular mechanism for RANKL expression. The findings of this study will provide a molecular basis for future pharmacological therapy of osteoporosis induced by mechanical unloading.