期刊
JOURNAL OF BONE AND MINERAL RESEARCH
卷 23, 期 8, 页码 1182-1193出版社
WILEY
DOI: 10.1359/JBMR.080310
关键词
calcitonin; knock-out/in; bone histomorphornetry
资金
- NCRR NIH HHS [S10 RR017868] Funding Source: Medline
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 CrelloxP system, in which the CTR is globally deleted by > 94% but < 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)(2)D-3] -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.
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