Abstract:
:Stimulators of bone resorption, such as PTH, 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], or prostaglandin E2 (PGE2), do not cause calcium release from cultured calvaria of the genetically determined osteopetrotic microphthalmic (mi/ mi) mouse, due to a defect in the function of osteoclasts. To investigate the capacity of cells of mi/mi bone to degrade collagen, calvaria of 1- to 3-day-old normal and mi/mi littermates were labeled in vivo with [3H]proline 16 h before removal, followed by culture in resorption medium. PTH, 1,25-(OH)2D3, and PGE2 stimulated the release of 3H-labeled material into the culture medium from both normal and mi/mi calvaria. The labeled substance released was of collagenous origin, as indicated by its content of hydroxyproline and susceptibility to collagenase. PTH also stimulated the release of 3H-labeled materials from normal calvaria labeled in vivo 112 h before the mice were killed, but had little or no effect on 3H release from the mi/mi bone, indicating that only noncalcified collagen is susceptible to hormone-stimulated degradation in osteopetrotic bone. We conclude that a portion of the hormone-stimulated resorptive mechanism, namely collagenolysis, is functional in bone of mi/mi mice. This result helps to pinpoint the resorptive defect in mi/ mi bone to a failure to dissolve mineral, rather than a more general phenomenon of failure to remove both mineral and matrix.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Jilka RL,Cohn DVdoi
10.1210/endo-112-3-945subject
Has Abstractpub_date
1983-03-01 00:00:00pages
945-50issue
3eissn
0013-7227issn
1945-7170journal_volume
112pub_type
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