Journal article
The role of the calcitonin receptor in protecting against induced hypercalcemia is mediated via its actions in osteoclasts to inhibit bone resorption
AG Turner, F Tjahyono, WSM Chiu, J Skinner, R Sawyer, AJ Moore, HA Morris, DM Findlay, JD Zajac, RA Davey
Bone | Published : 2011
Abstract
Despite the therapeutic value of calcitonin in treating bone disease, a biological role of endogenous calcitonin is controversial. Having previously demonstrated that the CTR has a biological role in protecting against calcium stress using a global CTRKO mouse model, the purpose of this study was to determine whether the protection conferred by the CTR during induced hypercalcemia is mediated via CTR expression on osteoclasts. Mice were generated, in which the CTR was deleted specifically within osteoclasts (OCL-CTRKOs) and compared with mice in which the CTR was deleted globally (global CTRKOs). Significantly, peak serum calcium levels following induced hypercalcemia were > 18% higher in gl..
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Grants
Awarded by National Health and Medical Research Council
Funding Acknowledgements
The authors thank Patricia Russell and Michele Milne of the University of Melbourne, Australia for their excellent technical assistance and Dr Mary Bouxsein of the Beth Israel Deaconess Medical Center and Harvard Medical School, USA for the cortical bone microCT analyses. This work was supported by the National Health and Medical Research Council of Australia (Project Grant 454484) and The Austin Hospital Medical Research Foundation.