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    Parathyroid-responsive modifications in the nuclear matrix of ROS 17/2.8 rat osteosarcoma cells

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    Authors
    Bidwell, Joseph P.
    Van Wijnen, Andre J.
    Banerjee, Chaitali
    Fey, Edward G.
    Merriman, Harold L.
    Penman, Sheldon
    Stein, Janet L.
    Lian, Jane B.
    Stein, Gary S.
    UMass Chan Affiliations
    Department of Cell Biology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    1994-04-01
    Keywords
    Animals; Antigens, Nuclear; Carcinoma, Hepatocellular; Cell Division; Nuclear Matrix; Nuclear Proteins; Osteoblasts; Osteosarcoma; Parathyroid Hormone; Phenotype; Rats; Transcription, Genetic; Tumor Cells, Cultured
    Life Sciences
    Medicine and Health Sciences
    
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    https://doi.org/10.1210/endo.134.4.8137738
    Abstract
    PTH is a mediator of skeletal development and remodeling that influences gene expression in osteoblastic cells. It is well established that PTH modulates the activity of membrane-associated second messenger signal transduction pathways. In these studies we have addressed the potential contribution of components of cell structure to the integration of PTH-related regulatory signals that influence the expression of bone cell genes. Chronic treatment of ROS 17/2.8 rat osteosarcoma cells with PTH is accompanied by changes in gene expression that are at least in part transcriptionally controlled. To explore the involvement of nuclear architecture in PTH-responsive modifications in gene expression, we investigated changes in the nuclear matrix after PTH treatment. Consistent with a role for the nuclear matrix in determining spatial organization and topology of chromatin as well as in the localization and targeting of transcription factors, we observed PTH-associated changes in a 200-kilodalton nuclear matrix protein in response to PTH. A significant down-regulation of synthesis was observed when nuclear matrix proteins were resolved electrophoretically in two-dimensional gels. This protein was restricted to the nuclear matrix and was not detected in the chromatin or cytoskeletal cellular fractions. These alterations in nuclear matrix proteins that occur after PTH treatment in osteosarcoma cells were phenotype related. They did not occur in UMR-106 POL or H4 hepatoma cells. Our findings support a role for the nuclear matrix in transducing PTH-mediated regulatory signals to facilitate the extent to which genes in osteoblasts are transcribed.
    Source

    Endocrinology. 1994 Apr;134(4):1738-44.

    DOI
    10.1210/endo.134.4.8137738
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34331
    PubMed ID
    8137738
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    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1210/endo.134.4.8137738
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