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Glucocorticoids and the plasma membrane.

T D Gelehrter

    Monographs on Endocrinology
    |January 1, 1979
    PubMed
    Summary

    Glucocorticoids, like dexamethasone, alter cell membrane transport and reduce plasminogen activator production in rat hepatoma cells. This hormonal effect requires protein synthesis and involves later steps in hormone action.

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    Area of Science:

    • Cell Biology
    • Endocrinology
    • Molecular Biology

    Background:

    • Glucocorticoids influence plasma membrane composition and function across various cell types.
    • Cultured rat hepatoma (HTC) cells serve as a model to study these glucocorticoid-induced effects.
    • Dexamethasone is a potent synthetic glucocorticoid used in research.

    Purpose of the Study:

    • To investigate the effects of dexamethasone on amino acid transport and plasminogen activator production in HTC cells.
    • To explore the mechanisms underlying glucocorticoid-mediated inhibition of these cellular functions.
    • To isolate and characterize dexamethasone-resistant cell variants to understand hormone action pathways.

    Main Methods:

    • Utilized cultured rat hepatoma (HTC) cells for experiments.
    • Assessed amino acid influx using the A or alanine-preferring transport system.
    • Employed an agar-fibrin overlay technique to detect plasminogen activator production and isolate resistant variants.
    • Investigated the requirement for protein synthesis and the role of cytoskeletal elements.

    Main Results:

    • Dexamethasone rapidly inhibited amino acid influx and decreased microvilli, while increasing cell adhesiveness.
    • Continuous protein synthesis was necessary for glucocorticoid inhibition of transport.
    • Dexamethasone significantly reduced plasminogen activator production.
    • Isolated cell variants resistant to dexamethasone's effect on protease production maintained other glucocorticoid-regulated functions.

    Conclusions:

    • Glucocorticoid action involves specific, later steps in hormone signaling pathways, particularly for regulating plasminogen activator.
    • Genetic and biochemical analysis of resistant variants can elucidate hormonal regulation of membrane phenotypes and protease roles.
    • HTC cells provide a valuable model for dissecting glucocorticoid-regulated cellular processes.

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