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   <subfield code="a">10.1007/s00774-014-0568-8</subfield>
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   <subfield code="a">Hindlimb-unloading suppresses B cell population in the bone marrow and peripheral circulation associated with OPN expression in circulating blood cells</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Yoichi Ezura, Junji Nagata, Masashi Nagao, Hiroaki Hemmi, Tadayoshi Hayata, Susan Rittling, David Denhardt, Masaki Noda]</subfield>
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   <subfield code="a">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.</subfield>
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  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">The Japanese Society for Bone and Mineral Research and Springer Japan, 2014</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Osteopontin</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Tail-suspension</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hindlimb unloading</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">PBMC</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Lymphocyte fraction</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Ezura</subfield>
   <subfield code="D">Yoichi</subfield>
   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Nagata</subfield>
   <subfield code="D">Junji</subfield>
   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Nagao</subfield>
   <subfield code="D">Masashi</subfield>
   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
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   <subfield code="a">Hemmi</subfield>
   <subfield code="D">Hiroaki</subfield>
   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
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   <subfield code="a">Hayata</subfield>
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   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
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   <subfield code="a">Rittling</subfield>
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   <subfield code="u">The Forsyth Institute, The Fenway, 02115, Boston, MA, USA</subfield>
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   <subfield code="a">Denhardt</subfield>
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   <subfield code="u">Department of Cell Biology and Neuroscience, Rutgers University, 08854, Piscataway, NJ, USA</subfield>
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   <subfield code="a">Noda</subfield>
   <subfield code="D">Masaki</subfield>
   <subfield code="u">Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 5-45 Yushima 1-Chome, Bunkyo-ku, 113-8510, Tokyo, Japan</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Journal of Bone and Mineral Metabolism</subfield>
   <subfield code="d">Springer Japan</subfield>
   <subfield code="g">33/1(2015-01-01), 48-54</subfield>
   <subfield code="x">0914-8779</subfield>
   <subfield code="q">33:1&lt;48</subfield>
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   <subfield code="z">Onlinezugriff via DOI</subfield>
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   <subfield code="a">BK010053</subfield>
   <subfield code="b">XK010053</subfield>
   <subfield code="c">XK010000</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="F">NATIONALLICENCE</subfield>
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