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Circulating factors controlling cell proliferation.

J C Houck

    Progress in Clinical and Biological Research
    |January 1, 1976
    PubMed
    Summary
    This summary is machine-generated.

    Fibroblast proliferation is regulated by an endogenous inhibitor (chalone) and a serum-derived mitogen that compete for cell surface binding. This interaction controls fibroblast growth in a reciprocal manner.

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    Area of Science:

    • Cell Biology
    • Biochemistry
    • Molecular Biology

    Background:

    • Diploid human fibroblasts require serum for proliferation, unlike other fibroblast types.
    • Fibroblast-rich tissues contain endogenous macromolecules that inhibit fibroblast proliferation.

    Purpose of the Study:

    • To investigate the nature of fibroblast proliferation inhibitors and mitogens.
    • To elucidate the mechanism of fibroblast growth regulation by serum components and endogenous factors.

    Main Methods:

    • Ultrafiltration, isoelectric focusing, and preparative polyacrylamide gel electrophoresis were used to purify serum mitogens.
    • Enzyme digestion (trypsin, RNase, DNase) and thermal stability tests characterized the endogenous inhibitor.
    • Cell-based assays measured proliferation inhibition and mitogenic activity, along with in vitro and in vivo studies.

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    Main Results:

    • An endogenous fibroblast inhibitor (chalone) was identified, with molecular weight 30-50 kDa, destroyed by trypsin, thermolabile, and acidic.
    • A purified serum mitogen (100 kDa) was isolated, composed of two 60 kDa subunits, containing sialic acid, S-S bonds, and hexose.
    • The mitogen and inhibitor exhibited reciprocal biological activity, suggesting a competitive interaction.

    Conclusions:

    • Fibroblast proliferation is controlled by a chalone-inhibitor and a serum anti-chalone (mitogen) that compete for cell surface binding.
    • This competitive interaction regulates fibroblast growth, with serum mitogen release correlating with chalone release.
    • The findings propose a novel mechanism for fibroblast growth control involving reciprocal interactions between endogenous and exogenous factors.