骨恒常性の維持における局所カルシウム輸送とビタミンDの役割(若手シンポジウム「ビタミン基礎研究の進展を担う若手研究者たち」,<特集>ビタミン基礎研究の進展を担う若手研究者たち(第64回大会若手シンポジウム))

  • 増山 律子
    長崎大学大学院医歯薬学総合研究科分子硬組織生物学分野

書誌事項

タイトル別名
  • Local calcium transport and role of vitamin D in maintaining bone homeostasis
  • 骨恒常性の維持における局所カルシウム輸送とビタミンDの役割
  • ホネ コウジョウセイ ノ イジ ニ オケル キョクショ カルシウム ユソウ ト ビタミン D ノ ヤクワリ

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抄録

A major disadvantage of a systemic VDR-null mouse model is that the expected 1,25 dihydroxy vitamin D [1,25(OH)_2D] -mediated skeletal and renal adaptations to reduced intestinal calcium absorption do not occur, due to the lack of VDR activity in these tissues. Systemic VDR-null mice, therefore, are not an appropriate model to unravel the physiological repercussions of negative calcium balance (or lack of intestinal 1,25(OH)_2D activity) on calcium and bone homeostasis. Accordingly, we have generated tissue specific VDR-ablation to manipulate local 1,25(OH)_2D activity. Furthermore, calcium movement from bone after osteoclastic bone resorption is a large calcium supply to maintain calcium homeostasis, the system supporting calcium homeostasis in osteoclast has not yet been identified. Transient receptor potential vanilloid (TRPV) 4, mediates Ca^<2+>influx in the late stage of osteoclast differentiation and, thereby regulates Ca^<2+> signaling. However, the system-modifying effect of TRPV4 activity remains to be determined. To elucidate the consequences of insufficient intestinal calcium absorption on calcium and bone homeostasis, and how cellular calcium homeostasis has been regulated during bone remodeling, whether 1,25(OH)_2D or calcium homeostasis influences osteoclastogenesis should be solved as an important question

収録刊行物

  • ビタミン

    ビタミン 87 (1), 38-43, 2013

    公益社団法人 日本ビタミン学会

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