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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Biochemistry 15 (1976), S. 2130-2135 
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0827
    Keywords: Vitamin D metabolites ; Calcitriol ; Bone resorption ; Bone collagen synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We compared the effects of four vitamin D metabolites, 1α,25 dihydroxy vitamin D3 (1α,25(OH)2D3), 1α hydroxy vitamin D3 (1αOH D3), 25 hydroxy vitamin D3 (25 OH D3), and 24R,25 dihydroxy vitamin D (24R,25(OH)2D3) on resorption and collagen synthesis in fetal rat bone maintained in organ culture. Resorption was quantitated by measuring the release of previously incorporated45Ca from long bone shafts of 19-day fetal rats, and collagen synthesis was assessed by measuring the incorporation of3H-proline into collagenase digestible protein (CDP) in calvaria from 21-day fetal rats. All four compounds stimulated bone resorption and inhibited collagen synthesis, but 1α,25(OH)2D3 was approximately 1000 times more potent in both organ culture systems. Although the differences were small among the other three compounds, the order of potency was 1αOH D3〉25 OH D3≧24R,25(OH)2D3. These results suggest that the receptor for 1α25(OH)2D3 in both bone resorbing and bone forming cells has similar affinities for several vitamin D metabolites.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0827
    Keywords: 1,25-Dihydroxyvitamin D3 ; Bone matrix synthesis ; Autoradiography ; [3H]proline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary An autoradiographic technique using pulse labels of [3H]proline was developed to assess the early effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on bone matrix synthesis in vitamin D replete rats. Rats, 7 days old, were given 0.25, 2.5, or 25 ng of 1,25(OH)2D3 or vehicle alone subcutaneously on days 1, 3, and 5 of the experiment. Rats received a subcutaneous injection of 100 µCi [3H]proline on days 2 and 6 and were killed on day 7. Calvaria and tibia were processed for autoradiography, and morphometric methods were developed to measure the rate and amount of bone matrix formed during the experimental period. When compared to control values, the amount and rate of formation of new bone matrix were both significantly decreased in rats receiving 25 ng of 1,25(OH)2D3 and slightly, but not significantly, decreased in rats receiving 2.5 ng. We conclude that administration of pharmacologic doses of 1,25(OH)2D3 to vitamin D replete rat pups impairs the formation of collagenous bone matrix.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 34 (1982), S. 370-375 
    ISSN: 1432-0827
    Keywords: Complement ; Bone ; Collagen ; Prostaglandins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Activation of rabbit serum complement caused a marked reduction in collagen synthesis but a much smaller change in noncollagen protein synthesis in fetal rat calvaria maintained in organ culture. In the periosteum of the fetal rat calvarium, both collagen and noncollagen protein synthesis were reduced, whereas in the central bone, presumably enriched in osteoblasts, only collagen synthesis was inhibited. This large decrease in bone collagen synthesis could not be attributed to enhanced degradation of newly synthesized collagen or its release into the culture medium. Activation of complement also stimulated the production of PGE in fetal rat calvaria. Antagonists of prostaglandin cyclooxygenase decreased prostaglandin synthesis but did not restore collagen synthesis in complement-treated bones, suggesting that complement decreases osteoblast collagen synthesis by a mechanism largely independent of prostaglandin production.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0730-2312
    Keywords: type I collagen ; gene regulation by steroid hormone ; bone cells in culture ; vitamin D ; nucleotides ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The synthesis of type 1 colagen in bone cells is inhibited by the calcium-regulating hormone 1,25-dihydroxyvitamin D3. Earlier work from our laboratoties has indicated that vitamin D regulation is at the level of transcription, based on result from both nuclear run-off assays and functional analysis of a hybrid gene consisting of a 3.6 kb COL1A1 promoter fragment fused to the chloraphenicol acetyltransferase reporter gene. In the present study, we investigated the molecular basis for vitamin D-mediated transcriptional repression of the COL1A1 gene and report the identification of a region within the COL1A1 upstream promoter (the Hindlll-Pstl restriction fragment between nucleotides-2295 and -1670) which is necessary for 1,25-dihydroxyvitamin D3 responsiveness in osteoblastic cells. This hormone-mediated inhibitory effect on the marker gene parallels the inhibition of the endogenous collagen gene. A 41 bp fragment from this region (between nucleotides-2256 and -2216) contains a sequence which is very similar to vitamin D-responsive elements identified in the osteocalcin gene. Estracts that binds specifically to this 41 bp fragment, as demonstrated by bandshift anslysis. However, deletion of this vitamin D receptor binding region from either a-3.5 kb or a-2.3 kb promoter fragment did not abolish vitamin D responsiveness. These results indicate that a vitamin D response element similar to that described for other D responsive genes (osteocalcin and osteopontin) does not alone mediate the repression of COL1A1 by 1,25-dihydroxyvitamin D3.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
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