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    Relationship of cell growth to the regulation of tissue-specific gene expression during osteoblast differentiation

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    Authors
    Stein, Gary S.
    Lian, Jane B.
    Owen, Thomas A.
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    1990-10-01
    Keywords
    Animals
    Base Sequence
    *Cell Differentiation
    *Cell Division
    Cells, Cultured
    *Gene Expression Regulation
    Histones
    Molecular Sequence Data
    Osteoblasts
    Phenotype
    Promoter Regions, Genetic
    RNA, Messenger
    Rats
    Cell Biology
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    Link to Full Text
    http://www.fasebj.org/content/4/13/3111.abstract
    Abstract
    The relationship of cell proliferation to the temporal expression of genes characterizing a developmental sequence associated with bone cell differentiation can be examined in primary diploid cultures of fetal calvarial-derived osteoblasts by the combination of molecular, biochemical, histochemical, and ultrastructural approaches. Modifications in gene expression define a developmental sequence that has 1) three principal periods: proliferation, extracellular matrix maturation, and mineralization; and 2) two restriction points to which the cells can progress but cannot pass without further signals. The first restriction point is when proliferation is down-regulated and gene expression associated with extracellular matrix maturation is induced, and the second when mineralization occurs. Initially, actively proliferating cells, expressing cell cycle and cell growth regulated genes, produce a fibronectin/type I collagen extracellular matrix. A reciprocal and functionally coupled relationship between the decline in proliferative activity and the subsequent induction of genes associated with matrix maturation and mineralization is supported by 1) a temporal sequence of events in which an enhanced expression of alkaline phosphatase occurs immediately after the proliferative period, and later an increased expression of osteocalcin and osteopontin at the onset of mineralization; 2) increased expression of a specific subset of osteoblast phenotype markers, alkaline phosphatase and osteopontin, when proliferation is inhibited; and 3) enhanced levels of expression of the osteoblast markers when collagen deposition is promoted, suggesting that the extracellular matrix contributes to both the shutdown of proliferation and development of the osteoblast phenotype. The loss of stringent growth control in transformed osteoblasts and in osteosarcoma cells is accompanied by a deregulation of the tightly coupled relationship between proliferation and progressive expression of genes associated with bone cell differentiation.
    Source
    FASEB J. 1990 Oct;4(13):3111-23.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/49468
    PubMed ID
    2210157
    Related Resources
    Link to Article in PubMed
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    UMass Chan Faculty and Researcher Publications

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