Hindlimb-unloading suppresses B cell population in the bone marrow and peripheral circulation associated with OPN expression in circulating blood cells

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• 作者：Yoichi Ezura (1) (2)
  Junji Nagata (1)
  Masashi Nagao (1)
  Hiroaki Hemmi (1) (3)
  Tadayoshi Hayata (1)
  Susan Rittling (4)
  David T. Denhardt (5)
  Masaki Noda (1) (2) (6) (7)
  
  1. Department of Molecular Pharmacology ; Medical Research Institute ; Tokyo Medical and Dental University ; 5-45 Yushima 1-Chome ; Bunkyo-ku ; Tokyo ; 113-8510 ; Japan
  2. Hard Tissue Genome Research Center ; TMDU ; Tokyo ; Japan
  3. Medical Top Track Fellow Program (MTT) ; TMDU ; Tokyo ; Japan
  4. The Forsyth Institute ; The Fenway ; Boston ; MA ; 02115 ; USA
  5. Department of Cell Biology and Neuroscience ; Rutgers University ; Piscataway ; NJ ; 08854 ; USA
  6. Global Center of Excellence (GCOE) Program ; International Research Center for Molecular Science in Tooth and Bone Diseases ; Tokyo ; Japan
  7. Integrated Action Initiative in JSPS Core to Core Program ; Tokyo ; Japan
  
• 关键词：Osteopontin ; Tail ; suspension ; Hindlimb unloading ; PBMC ; Lymphocyte fraction
• 刊名：Journal of Bone and Mineral Metabolism
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：33
• 期：1
• 页码：48-54
• 全文大小：570 KB
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• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Metabolic Diseases
  Orthopedics
  Internal Medicine
  
• 出版者：Springer Japan
• ISSN：1435-5604

文摘

Rodent hindlimb unloading (HU) by tail-suspension is a model to investigate disuse-induced bone loss in vivo. Previously, we have shown that osteopontin (OPN, also known as Spp1) is required for unloading-induced bone loss. However, how unloading affects OPN expression in the body is not fully understood. Here, we examined OPN expression in peripheral blood of mice subjected to HU. Real-time RT-PCR analysis indicated that OPN expression is increased in circulating peripheral blood cells. This HU-induced increase in OPN mRNA expression was specific in circulating peripheral blood cells, as OPN was not increased in the blood cells in bone marrow. HU-induced enhancement in OPN expression in peripheral blood cells was associated with an increase in the fraction of monocyte/macrophage lineage cells in the peripheral blood. In contrast, HU decreased the fraction size of B-lymphocytes in the peripheral blood. We further examined if B-lymphogenesis is affected in the mice deficient for osteopontin subjected to HU. In bone marrow, HU decreased the population of the B-lymphocyte lineage cells significantly, whereas it did not alter the population of monocyte/macrophage lineage cells. HU also increased the cells in T-lymphocyte lineage in bone marrow. Interestingly, these changes were observed similarly both in OPN-deficient and wild-type mice. These results indicate for the first time that HU increases OPN expression in circulating cells and suppresses bone marrow B-lymphogenesis.