DIFFERENTIAL REGULATION OF INSULIN-LIKE GROWTH FACTOR-I (IGF-I) AND IGF-II RELEASE FROM CULTURED NEONATAL MOUSE CALVARIA BY PARATHYROID-HORMONE, TRANSFORMING GROWTH-FACTOR-BETA, AND 1,25-DIHYDROXYVITAMIN-D3

被引:69
作者
LINKHART, TA
KEFFER, MJ
机构
[1] LOMA LINDA UNIV,SCH MED,DEPT BIOCHEM,LOMA LINDA,CA 92354
[2] LOMA LINDA UNIV,SCH MED,DEPT PEDIAT,LOMA LINDA,CA 92354
关键词
D O I
10.1210/endo-128-3-1511
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In a previous study we found that PTH stimulated bone resorption and release of insulin-like growth factor-I (IGF-I) and IGF-II from cultured neonatal mouse calvaria. Since IGF-I and IGF-II stimulate osteoblast proliferation and collagen synthesis, these results suggested that increased release of IGFs during resorption could mediate in part coupling of bone formation to bone resorption. In the present study two other osteolytic agents, transforming growth factor-beta (TGF-beta) and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3 were examined for effects on IGF release from neonatal mouse calvaria. Like PTH, TGF-beta stimulated resorption and increased release of IGF-I and IGF-II, 1,25-(OH)2D3, however, stimulated resorption and IGF-II release comparable to PTH, but inhibited release of IGF-I. 1,25-(OH)2D3 (0.1-100 nM) inhibited basal release of IGF-I, and 10 nM 1,25-(OH)2D3 inhibited release of IGF-I induced by PTH or TGF-beta. The effects of 1,25-(OH)2D3 were specific to this vitamin D metabolite and did not occur with 25-hydroxyvitamin D3 or 24,25-(OH)2D3 at the same concentration. Calcitonin (50 mU/ml) decreased 1,25-(OH)2D3 stimulation of resorption, but did not affect 1,25-(OH)2D3 stimulation of IGF-II release and inhibition of IGF-I release. This evidence that effects of 1,25-(OH)2D3 on release of the IGFs were independent of bone resorption supports the conclusion that 1,25-(OH)2D3 modulated the production and secretion of IGF-I and IGF-II in calvarial cells. The results of this and the previous study suggest that PTH, TGF-beta, and 1,25-(OH)2D3 differentially regulate mouse calvarial cell IGF-I and IGF-II production.
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页码:1511 / 1518
页数:8
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