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  • Articles  (57)
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  • Articles  (57)
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  • 1
    Electronic Resource
    Electronic Resource
    Effect of multiplication-stimulating activity on DNA and protein synthesis in cultured fetal rat calvaria (1979)
    Springer
    Calcified tissue international 29 (1979), S. 33-39 
    Details
    ISSN: 1432-0827
    Keywords: Multiplication-stimulating activity ; Somatomedin ; Tissue culture ; Bone formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Multiplication-stimulating Activity (MSA), a peptide closely related to somatomedin, was examined for its effects on bone formation and sulfation activity in vitro. To study the effect of MSA on bone formation, we examined its effects on the incorporation of3H-thymidine into DNA,3H-uridine into RNA, and3H-proline into collagenase-digestible (CDP) and noncollagen protein (NCP), as well as DNA content in 21-day fetal rat calvaria cultured for 24 h periods. MSA caused a dose-dependent stimulation of the incorporation of3H-thymidine into DNA at concentrations of 1 to 3µg/ml, increased the total DNA content, and had no effect on3H-uridine incorporation. The effect on3H-thymidine incorporation appeared and was maximal at 12 h and was sustained for 24 h. After 24 h of treatment, MSA, 1 to 3µg/ml, caused a 25 to 60% stimulation on the incorporation of3H-proline into CDP and NCP. The effect was not specific for CDP, and there was no increase in the percent collagen synthesized. In contrast, insulin, 10 nM, increased the labeling of CDP by 95% but had a small effect on NCP and did not affect DNA synthesis. Insulin did not diminish the MSA effect on CDP and NCP labeling but slightly decreased its effect on thymidine incorporation. Cortisol inhibited DNA synthesis, but MSA was effective in its presence and cortisol did not affect the stimulatory effect of MSA on CDP or NCP. Histological sections showed a sixfold increase in the mitotic index after colcemid arrest in MSA-treated bones. MSA, 0.1 to 5µg/ml, also stimulated the incorporation of35S into pig costal cartilage in culture. Our studies indicate that MSA stimulates DNA, collagen, and noncollagen protein synthesis in bone cultures and stimulates sulfate incorporation into cartilage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408053
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of sex steroids on bone collagen synthesis in vitro (1978)
    Springer
    Calcified tissue international 25 (1978), S. 105-110 
    Details
    ISSN: 1432-0827
    Keywords: Progesterone ; 17β estradiol ; Testosterone ; Tissue culture ; Bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Although sex steroids are known to affect skeletal metabolism, their effects on bone collagen synthesis have not been studied. We have examined the direct effects of progesterone, 17β estradiol, testosterone, 5α dihydrotestosterone and dehydroepiandrosterone on bone collagen and noncollagen protein synthesis in cultures of calvaria obtained from 21-day fetal rats. Bones were incubated for 24 to 168 h and3H-proline was added for the last 2 h of culture. Incorporation of the label into collagenase-digestible protein (CDP)1 and noncollagen protein (NCP) was determined using repurified bacterial collagenase. Progesterone caused a dose dependent inhibition of the labeling of CDP at concentrations of 3×10−7 M to 10−5 M after 96 h of culture. A smaller inhibitory effect was observed on NCP. The inhibitory effect was slow in onset and persisted when bones were incubated for 48 h with progesterone and then transferred to control medium for 48 h. Progesterone also inhibited the incorporation of3H-thymidine and3H-uridine into fetal rat calvaria. After 24 h of culture, 17β estradiol and testosterone had no effects on the labeling of CDP and NCP. After 96 h, 17β estradiol had a small and inconsistent stimulatory effect on the labeling of CDP but testosterone had no effect. Neither hormone altered the inhibitory effects of parathyroid hormone, cortisol and progesterone. Dihydrotestosterone and dehydroepiandrosterone had no effects after 24 h and 96 h of culture. 17β estradiol, testosterone and dihydrotestosterone did not affect the incorporation of3H-uridine or3H-thymidine into fetal rat calvaria. Our studies indicate that progesterone is an inhibitor of bone collagen synthesis and estrogens and androgens are not major regulators of bone formation in vitro.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02010758
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of cartilage-derived factor on DNA and protein synthesis in cultured rat calvariae (1984)
    Springer
    Calcified tissue international 36 (1984), S. 102-107 
    Details
    ISSN: 1432-0827
    Keywords: Cartilage-derived factor ; DNA ; Collagenase-digestible protein ; Noncollagen protein-Calvarial
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Cartilage-derived factor (CDF), a peptide closely related to the somatomedins, was studied for its effects on bone formation by examining the synthesis of DNA, collagen, and noncollagen protein in 24–96 h cultures of 21-day fetal rat calvariae. After 24 h of treatment, CDF at concentrations of 0.3–30 µg/ml caused a dose-dependent stimulation of the incorporation of3H-thymidine into DNA by 12–59%. The effect appeared and was maximal after 12 h, and was sustained for 96 h. CDF also increased the bone DNA content by 30–60%. After 24 h of treatment, CDF at 10–30 µg/ml had a small stimulatory effect on the incorporation of3H-proline into collagenase-digestible protein (CDP) and noncollagen protein (NCP). The effect on the labeling of CDP and NCP was sustained for 96 h. Cortisol decreased the stimulatory effect of CDF on DNA labeling but cortisol and CDF had an additive effect on the incorporation of3H-proline into CDP. The CDF stimulatory effect on the labeling of DNA, CDP, and NCP was seen in both the periosteum and periosteum-free calvaria. These studies indicate that CDF stimulates bone DNA, collagen, and noncollagen protein synthesisin vitro and may be a local regulator of bone growth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405301
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  • 4
    Electronic Resource
    Electronic Resource
    Local bone growth factors (1984)
    Springer
    Calcified tissue international 36 (1984), S. 632-634 
    Details
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405381
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of cortisol on periosteal and nonperiosteal collagen and DNA synthesis in cultured rat calvariae (1984)
    Springer
    Calcified tissue international 36 (1984), S. 158-166 
    Details
    ISSN: 1432-0827
    Keywords: Cortisol ; Collagen synthesis ; DNA synthesis ; Alkaline phosphatase activity ; Periosteum and nonperiosteal bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effects of cortisol on bone formation are complex and may be modulated by the presence of periosteal cells or by factors released by the periosteal tissue. To test these possibilities, cortisol was examined for its effects on the incorporation of3H-proline into collagenase-digestible protein (CDP) and noncollagen protein (NCP), on DNA synthesis and on alkaline phosphatase activity in intact and in the periosteum and nonperiosteal bone of dissected calvariae from 21-day-old fetal rats. After 24 h of treatment, cortisol increased the incorporation of3H-proline into CDP in intact bones and in the nonperiosteal bone of calvariae dissected after the culture. Cortisol inhibited the incorporation of3H-thymidine into calvarial DNA but it caused a small increase in nonperiosteal DNA content. Cortisol did not affect the incorporation of3H-proline into CDP in calvariae dissected prior to the culture if the periosteum and nonperiosteal central bone were incubated separately; the stimulatory effect was observed only if the two tissues were cultured in the same vial and were in contact. In contrast, cortisol stimulated alkaline phosphatase activity in the central nonperiosteal bone of calvariae dissected before or after the culture. After 72–96 h of treatment, cortisol inhibited the labeling of CDP, NCP, and DNA and the DNA content in intact bones and in both periosteal and nonperiosteal central bone of calvariae dissected after the culture. In contrast, when the periosteum was removed before the incubation, these inhibitory effects were observed in the periosteum and not in the nonperiosteal bone. Cortisol inhibited alkaline phosphatase activity in intact bones treated for 96 h, but removal of the periosteum resulted in a stimulatory effect in the nonperiosteal central bone. These studies indicate that 24 h treatment with cortisol stimulates collagen synthesis in nonperiosteal bone, an effect that requires the presence of periosteal tissue. Exposure to cortisol for 72–96 h inhibits collagen, noncollagen protein, and DNA synthesis, an effect that is secondary to an inhibition of periosteal cell replication. Cortisol does not cause a direct inhibition of osteoblastic function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405312
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  • 6
    Electronic Resource
    Electronic Resource
    Systemic and local factors and the maintenance of bone quality (1993)
    Springer
    Calcified tissue international 53 (1993), S. S90 
    Details
    ISSN: 1432-0827
    Keywords: Growth factors ; Hormones ; Bone formation ; Osteoblast
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Bone formation, an essential process for the maintenance of bone mass and strength, depends on changes in osteoblast number or function. Bone formation is modified by systemic hormones such as parathyroid hormone, growth hormone, insulin and steroids, and by local factors that act in an antocrine or paracrine fashion on the osteoblast. Skeletal cells synthesize platelet-derived growth factors and fibroblast growth factors, agents which affect osteoblast cell replication. In addition, skeletal cells synthesize insulin-like growth factors and transforming growth factors beta, agents which also affect the differentiated function of the osteoblast. Systemic and local factors that modify bone formation are likely critical in the maintenance of normal bone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01673411
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  • 7
    Electronic Resource
    Electronic Resource
    Mechanisms of glucocorticoid action in bone cells (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 295-302 
    Details
    ISSN: 0730-2312
    Keywords: osteoblast ; osteoporosis ; insulin-like growth factor ; collagen ; matrix metalloproteinase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Glucocorticoids play an important role in the normal regulation of bore remodeling; however continued exposure of bone to glucocorticoid excess results in osteoporosis. In vivo, glucocorticoids stimulate bone resorption and decreasae bone formation, and in vitro studies have shown that while glucocorticoids stimulateosteoblastic differentiation, they have important inhibitory actions on bone formation. Glucocorticoids have manyeffects on osteoblast gene expression, including down-regulation of type 1 collagen and osteocalcin, and up-regulation of interstitial collagenase. The synthesis and activity of osteoblast growth factors can be modulated by glucocorticoids as well. For example, insulin-like growth factor 1 (IGF-1) is an important stimulator of osteoblast function, and expression of IGF-1 is decreased by glucocorticoids. The activity of IGF 1 can be modified by IGF binding proteins (IGFBPs), and theirsynthesis is also regulated by glucocorticoids. Thus, glucocorticoid action on osteoblasts can be direct, by activating or repressing osteoblast gene expression, or indirect by altering the expression or activity of osteoblast growth factors. Further investigation of the mechanisms by which glucocorticoids mnodulate gene expression in bore cells will contribute to our understanding or steroid hormone biology and will provide a basis for the design of effective treatments for glucocorticoid-induced osteoporosis.
    Additional Material: 3 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560304
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  • 8
    Electronic Resource
    Electronic Resource
    Growth factor regulation of insulin-like growth factor binding protein-6 expression in osteoblasts (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 77-86 
    Details
    ISSN: 0730-2312
    Keywords: skeletal cells ; transforming growth factor &Bgr ; transcripts ; bone formation ; local factors ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Previously we have shown that transforming growth factor β (TGF β) 1, basic fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF) BB inhibit the synthesis of insulin-like growth factor (IGF) II, but their effects on IGF binding protein (IGFBP)-6 in osteoblast cultures are not known. IGFBP-6 binds IGF II with high affinity and prevents IGF II-mediated effects, so that a possible mode of regulating the IGF II available to bone cells would be by changing the levels of IGFBP-6. To enhance our understanding of the actions of growth factors on the IGF II axis in bone, we tested the effects of TGF β1, basic FGF, PDGF BB, IGF I, and IGF II on the expression of IGFBP-6 in cultures of osteoblast-enriched cells from 22 day fetal rat calvariae (Ob cells). Treatment of Ob cells with TGF β1 caused a time- and dose-dependent decrease in IGFBP-6 mRNA levels, as determined by Northern blot analysis. The effect was maximal after 48 h and observed with TGF β1 concentrations of 0.04 nM and higher. TGF β1 also decreased IGFBP-6 polypeptide levels in the medium, as determined by Western immunoblot analysis. Cycloheximide at 3.6 μM decreased IGFBP-6 transcripts and prevented the effect of TGF β1. The decay of IGFBP-6 mRNA in transcriptionally arrested Ob cells was not modified by TGF β1. In addition, TGF β1 decreased the rates of IGFBP-6 transcription as determined by a nuclear run-on assay. In contrast, basic FGF, PDGF BB, IGF I, and IGF II did not change IGFBP-6 mRNA levels in Ob cells. In conclusion, TGF β1 inhibits IGFBP-6 expression in Ob cells by transcriptional mechanisms. Since IGFBP-6 binds IGF II and prevents its effects on bone cells, decreased synthesis of IGFBP-6 induced by TGF β1 could be a local feedback mechanism to increase the amount of IGF II available in the bone microenvironment. J. Cell. Biochem. 66:77-86, 1997. © 1997 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
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  • 9
    Electronic Resource
    Electronic Resource
    Cellular and clinical perspectives on skeletal insulin-like growth factor I (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 55 (1994), S. 328-333 
    Details
    ISSN: 0730-2312
    Keywords: insulin-like growth factor I ; transcriptional control ; posttranscriptional control ; gene expression ; insulin-like growth factor binding proteins ; osteoblast ; bone formation ; osteoporosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin-like growth factor (IGF) I, a polypeptide synthesized by skeletal cells, is presumed to act as an autocrine regulator of bone formation. IGF I stimulates bone replication of preosteoblastic cells and enhances the differentiated function of the osteoblast. The synthesis of skeletal IGF I is regulated by systemic hormones, most notably parathyroid hormone and glucocorticoids, as well as by locally produced factors, such as prostaglandins and other skeletal growth factors. Whereas hormones and growth factors regulate IGF I synthesis, the exact level of regulation has not been established and may involve both transcriptional and posttranscriptional mechanisms. The IGF I gene contains six exons, and both exon 1 and 2 contain transcription initiation sites. Extrahepatic tissues, including bone, express exon 1 transcripts, and regulation of the exon 1 promoter activity in osteoblasts is currently under study. It is apparent that the regulation of IGF I gene transcription as well as the regulation of mRNA stability is complex and tissue specific. It is possible that abnormalities in skeletal IGF I synthesis or activity play a role in the pathogenesis of bone disorders. In view of its important anabolic actions in bone, it is tempting to postulate the use of IGF I for the treatment of disorders characterized by decreased bone mass. An alternative could be the stimulation of the local production of IGF I in bone. © 1994 Wiley-Liss, Inc.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240550309
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  • 10
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor I inhibits the transcription of collagenase 3 in osteoblast cultures (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 176-183 
    Details
    ISSN: 0730-2312
    Keywords: bone matrix ; collagen ; growth factors ; interstitial collagenase ; matrix metalloproteinases ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin-like growth factor (IGF) I is an autocrine regulator of bone remodeling which inhibits bone collagen degradation and interstitial collagenase 3 mRNA levels. The mechanism of this inhibitory effect on collagenase 3 expression is not known. We tested the effects of IGF I on collagenase 3 gene expression in cultures of osteoblast-enriched cells from 22 day fetal rat calvariae (Ob cells) to determine whether transcriptional or posttranscriptional mechanisms were involved in the regulation of the collagenase 3 gene. IGF I at 10-100 nM caused a dose-dependent decrease in collagenase mRNA and protein levels. IGF I did not modify the half-life of collagenase 3 mRNA in transcriptionally arrested Ob cells, whereas it decreased the levels of interstitial collagenase 3 heterogeneous nuclear RNA. In addition, IGF I decreased the rates of transcription of the collagenase gene and the activity of a 2.1 kilobase collagenase 3 promoter construct transiently transfected into Ob cells. In conclusion, IGF I decreases the expression of collagenase 3 mRNA by transcriptional mechanisms. J. Cell. Biochem. 67:176-183, 1997. © 1997 Wiley-Liss, Inc.
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