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1 Department of Animal Science, Molecular, Cellular, and Developmental Biology Program, Iowa State University Ames 50011
2 USDA, Agricultural Research Service, National Animal Disease Center, Metabolic Diseases and Immunology Research Unit Ames, IA 50010-0070
Cells of the monocyte-macrophage lineage have been thought to play a role in bone resorption. We examined the effects of in vitro administration of parathyroid hormone and 1,25-dihydroxyvitamin D3 on the ability of monocytes to degrade bone in vitro. Administration of parathyroid hormone for 4 d resulted in sustained hypercalcemia and a transient 1-d increase in plasma 1,25-dihydroxyvitamin D3. Parathyroid hormone significantly stimulated bone degradation by monocytes 2.6 times more than that of pretreatment controls. Parathyroid hormone treatment significantly enhanced (threefold) release of superoxide anion by monocytes stimulated with phorbol 12-myristate 13-acetate and increased migration of monocytes to bone particles in vitro. Continuous 7-d infusion of 1,25-dihydroxyvitamin D3 (50 µg/d) elevated plasma 1,25-dihydroxyvitamin D3 until infusions were discontinued. Increased 1,25-dihydroxyvitamin D3 was associated with hypercalcemia, which continued for several days postinfusion. In vitro administration of 1,25-dihydroxyvitarnin D3 did not affect in vitro ability of monocytes to degrade bone. We concluded that in vitro administration of parathyroid hormone enhanced in vitro responsiveness of isolated monocytes in a manner consistent with a role for monocytes in bone remodeling. Furthermore, these data suggested that circulating monocytes could be a useful experimental model for further studies on parathyroid hormone responsiveness and bone resorption for the cow with milk fever.
Key Words: milk fever parathyroid hormone bone resorption vitamin D
Submitted on March 28, 1995
Accepted on July 21, 1995
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