Calcitonin Receptor Plays a Physiological Role to Protect Against Hypercalcemia in Mice

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  • Rachel A Davey
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Andrew G Turner
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Julie F McManus
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • WS Maria Chiu
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Francisca Tjahyono
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Alison J Moore
    Hanson Institute, IMVS, Adelaide, Australia
  • Gerald J Atkins
    Department of Orthopaedics and Trauma, University of Adelaide, Adelaide, Australia
  • Paul H Anderson
    Hanson Institute, IMVS, Adelaide, Australia
  • Cathy Ma
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Vaida Glatt
    Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
  • Helen E MacLean
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia
  • Cristina Vincent
    Hanson Institute, IMVS, Adelaide, Australia
  • Mary Bouxsein
    Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
  • Howard A Morris
    Hanson Institute, IMVS, Adelaide, Australia
  • David M Findlay
    Department of Orthopaedics and Trauma, University of Adelaide, Adelaide, Australia
  • Jeffrey D Zajac
    Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia

説明

<jats:title>Abstract</jats:title> <jats:p>It is well established that calcitonin is a potent inhibitor of bone resorption; however, a physiological role for calcitonin acting through its cognate receptor, the calcitonin receptor (CTR), has not been identified. Data from previous genetically modified animal models have recognized a possible role for calcitonin and the CTR in controlling bone formation; however, interpretation of these data are complicated, in part because of their mixed genetic background. Therefore, to elucidate the physiological role of the CTR in calcium and bone metabolism, we generated a viable global CTR knockout (KO) mouse model using the Cre/loxP system, in which the CTR is globally deleted by &gt;94% but &lt;100%. Global CTRKOs displayed normal serum ultrafiltrable calcium levels and a mild increase in bone formation in males, showing that the CTR plays a modest physiological role in the regulation of bone and calcium homeostasis in the basal state in mice. Furthermore, the peak in serum total calcium after calcitriol [1,25(OH)2D3]-induced hypercalcemia was substantially greater in global CTRKOs compared with controls. These data provide strong evidence for a biological role of the CTR in regulating calcium homeostasis in states of calcium stress.</jats:p>

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