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  • Cell & Developmental Biology  (3)
  • DNA synthesis  (1)
  • Epidermal growth factor  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Epidermal growth factor receptors in clonal lines of a rat osteogenic sarcoma and in osteoblast-rich rat bone cells (1983)
    Springer
    Calcified tissue international 35 (1983), S. 298-303 
    Details
    ISSN: 1432-0827
    Keywords: Epidermal growth factor ; Receptors ; Osteoblasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Studies were carried out to identify and characterize the receptors for epidermal growth factor (EGF) in osteoblast-rich newborn rat calvarial cells and in 4 clonal lines derived from a transplantable rat osteogenic sarcoma with a well-characterized osteoblast-like phenotype. The cells were grown in monolayer culture in replicate wells; 40,000–50,000 cpm125I-labeled mouse EGF with a specific activity of 100–120µCi/µg was added to each well. Binding studies were carried out at 37°C. Binding of125I-labeled EGF was specific, saturable, reversible, and pH dependent. Maximum binding occurred 2 h after addition of the tracer. Thereafter, cell-bound radioactivity decreased to reach a plateau of 15–20% of maximum binding at 24 h. This observation is consistent with internalization and processing of the receptor-hormone complex as has been shown with other EGF target cells. Scatchard analyses revealed a single class of high-affinity binding sites in the normal and malignant osteoblast-like cells. Dissociation constants (KD) in the clonal lines ranged from 2.3 × 10−10M to 4.7 × 10−10M with receptor number per cell ranging from 25,000 to 33,000. The calvarial cells had a KD of 2.0 × 10−10M with 14,000 receptors per cell. In both the normal and malignant cell strains, EGF was found to increase incorporation of3H-labeled thymidine into acid-precipitable macromolecules. EGF has been shown to stimulate bone resorption; however, studies in organ cultures have not identified the target cell for EGF. The present results point to an interaction of EGF with osteoblasts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405050
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation of DNA synthesis by epidermal growth factor in osteoblast-like cells (1983)
    Springer
    Calcified tissue international 35 (1983), S. 624-628 
    Details
    ISSN: 1432-0827
    Keywords: EGF ; DNA synthesis ; Osteoblasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Normal and malignant osteoblast-like cells in culture have been shown to possess specific, high affinity receptors for epidermal growth factor (EGF). In this study, the mitogenic response to EGF was examined in a clonal line of a rat osteogenic sarcoma (UMR 106) and in osteoblast-rich newborn rat calvarial cells. Twenty-four hour treatment of UMR 106 cells with EGF in doses ranging from 10−12 m to 2 × 10−8 m stimulated the incorporation of [3H]thymidine and DNA synthesis in a dose-dependent manner. This short-term stimulatory effect was sustained in long-term culture with a dose-dependent increase in cell proliferation by calvarial cells. A lag period of 8 h occurred before significant stimulation of [3H]thymidine incorporation was observed. Commitment to increased incorporation of [3H]thymidine required a minimum of 6 h continuous incubation with EGF. These results establish the osteoblast as a target cell for EGF action on bone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405105
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms by which cells of the osteoblast lineage control osteoclast formation and activity (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 357-366 
    Details
    ISSN: 0730-2312
    Keywords: osteoblasts ; osteoclasts ; hormones ; cytokines ; hemopoietic cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The cells of bone are of two lineages, the osteoblasts arising from pluripotential mesenchymal cells and osteoclasts from hemopoietic precursors of the monocyte-macrophage series. Resorption of bone by the multinucleate osteoclast requires the generation of new osteoclastsw and their activation. Many hormones and cytokines are able to promote bone resorption by influencing these processes, but they achieve this without acting directly on osteoclastws. Most evidence indicates that their actions are mediated by cells of the osteoblast lineage. Evidence for hormone-and cytokine-induced activation of osteoclasts requiring the mediation of osteoblasts comes from studies of rsorption by isolated osteoclasts. However, consistent evidence for a spiceific “activating factor” is lacking, and the argument is presented that the isolated osteoclast resorption assays have not been shown convincingly to be assays of osteoclast activation. The view is presented that osteoblast-mediated osteoclast activation is the result of several events in the microenvironment without necessarily requiring the existence of a spicific, essential osteoclast activator. On the other hand, a specific promoter of osteoclast differentiation does seem likely to be a product of cells of the stromal/osteoblast series. Evidence in facour of this comes from studies of osteoclast generation in co-cultures of osteoblast/stromal cells with hemopoietic cells. Conflicting view, maintaining that osteoclasts can develop from hemooietic cells without stromal intervention, might be explaind by varying criteria used in identification of osteoclasts. Osteoblastic and osteoclastic renewal, and the interactions of these lineages, are central to the process of bone remodeling.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560312
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  • 4
    Electronic Resource
    Electronic Resource
    Cell substratum modulates responses of preosteoblasts to retinoic acid (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 157 (1993), S. 243-252 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The aim of this study was to determine the role of ECM components of bone in regulating the differentiation and function of cells of the osteoblast lineage. Rat UMR 201 cells, phenotypically preosteoblast, were plated onto plastic tissue culture dishes or dishes coated with gelled type I collagen or reconstituted basement membrane (matrigel). Acute cell attachment assays showed that cells adhered to substrates in the following order: collagen 〉 matrigel ≫ plastic. Proliferation rate up to 96 hr were similar on each substrate. However, if cells were treated with 10-6 M retinoic acid (RA), proliferation rates were reduced compared with control for cells grown on collagen and matrigel but not on plastic. Morphological changes were matrix-specific; in subconfluent cultures, long thin processes were seen with cells grown on collagen and a pattern of interconnecting cell processes formed when cells were plated on matrigel. Striking differences were observed in the constitutive or RA-induced gene expression of cells grown on the different substrates. When cells plated on collagen were treated with RA, induction of mRNA for alkaline phosphatase (ALP) as well as ALP enzyme activity were much less than with cells grown on plastic. In contrast, RA treatment induced osteopontin (OP) mRNA expression more strongly in cells plated on collagen compared with plastic within 24 hr and this was maintained for 72 hr. RA treatment produced a two fold increase of pro-α 1(I) collagen mRNA in cells grown on plastic and matrigel but not in cells grown on collagen. Growth on collagen produced changes in the way UMR 201 cells responded to RA from which they did not fully recover in subsequent 48-hr growth periods on plastic. These results indicate that ECM components regulate the function of and are capable of modulating RA-induced differentiation of preosteoblasts. © 1993 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041570206
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  • 5
    Electronic Resource
    Electronic Resource
    Osteoblasts display receptors for and responses to leukemia-inhibitory factor (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 145 (1990), S. 110-119 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Specific binding of leukemia-inhibitory factor (LIF) to osteoblasts, but not multinucleated osteoclasts, was demonstrated by receptor autoradiography by *using cells isolated from newborn rat long bones. The clonal rat osteogenic sarcoma cells, UMR 106-06, which have several phenotypic properties of osteoblasts, expressed 300 LIF receptors per cell, with an apparent KD of 60 pM. Treatment of calvarial osteoblasts or UMR 106-01 cells with LIF resulted in a dose-dependent inhibition of plasminogen activator (PA) activity. Both calvarial osteoblasts and osteogenic sarcoma cells were shown by Western blotting and reverse fibrin autography to produce plasminogen activator inhibitor-1 (PAI-1), the production of which was increased by LIF treatment. Northern blot analysis revealed that LIF treatment resulted in a rapid (peak 1 hour), dose-dependent increase in mRNA for PAI-1. LIF treatment of the preosteoblast cell line, UMR 201, enhanced the alkaline phosphatase response of these cells to retinoic acid. Each of the osteoblast-like cell types (calvarial osteoblasts, UMR 106-06, and UMR 201) was shown to produce LIF by bioassay and, by using the polymerase chain reaction (PCR), was shown to express low levels of mRNA for LIF. These data establish that cells of the osteoblast lineage are targets for LIF action. The reported anabolic effects of this cytokine on bone formation in vivo could be related to inhibition of protease activity. LIF may be an important paracrine modulator in bone, or perhaps an autocrine one, based on the evidence for its production by osteoblasts and osteoblast-like cells.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041450116
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