Abstract：
:Although osteocalcin is the most abundant noncollagenous protein in bone, its role remains undefined. Recent studies have reported diametrically opposing responses in the vitamin D regulation of the mouse vs the human and rat osteocalcin genes. The aim of this study was to increase the understanding of these differences and further elucidate the physiological function and regulation of osteocalcin. Direct comparison of the regulation of both the endogenous mouse osteocalcin gene (mOC) and a human osteocalcin promoter-chloramphenicol acetyl transferase (hOC-CAT) reporter as integrated templates was undertaken in primary osteoblastic cultures from OSCAT transgenic mice. Expression of both genes was up-regulated with the onset of mineralization. Long-term chronic 1, 25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) treatment and acute (2 day) PTH treatment inhibited both mOC and hOC-CAT expression. At all stages of osteoblastic development studied, hOC-CAT was up-regulated by acute 1,25-(OH)(2)D(3), whereas mOC was unaffected or inhibited. Mouse osteopontin was strongly up-regulated by acute 1, 25-(OH)(2)D(3) treatment. Thus, the divergence of the osteocalcin responses to 1,25-(OH)(2)D(3) is specific for the osteocalcin gene and for an acute 1,25-(OH)(2)D(3) treatment regime. Elucidation of this unique aspect of bone physiology will provide valuable insights into the still incompletely understood roles of osteocalcin and 1, 25-(OH)(2)D(3) in bone.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Thomas GP,Bourne A,Eisman JA,Gardiner EMdoi
10.1006/excr.2000.4912keywords:
subject
Has Abstractpub_date
2000-08-01 00:00:00pages
395-402issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(00)94912-7journal_volume
258pub_type
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journal_title：Experimental cell research
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