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Tumour promoter uncouples beta-adrenergic receptor from adenyl cyclase in mouse epidermis

S J Garte, S Belman

    Nature
    |March 13, 1980
    PubMed

    Insights

    Phorbol myristate acetate (PMA), a tumor promoter, disconnects skin cell beta-receptors from adenylate cyclase. This uncoupling inhibits cyclic AMP production without affecting basal levels or receptor numbers.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Dermatology

    Background:

    • Transformed cells and tumors exhibit altered beta-adrenergic receptor function and adenylate cyclase responsiveness.
    • Phorbol myristate acetate (PMA) is a potent tumor promoter in mouse skin.
    • PMA induces significant loss of epidermal responsiveness to catecholamines in vivo.

    Purpose of the Study:

    • To investigate the mechanism by which PMA inhibits epidermal responsiveness to catecholamines.
    • To determine if PMA affects beta-adrenergic receptor number, affinity, or coupling to adenylate cyclase.

    Main Methods:

    • Treatment of mouse skin with Phorbol myristate acetate (PMA).
    • Assessment of epidermal responsiveness to catecholamines (e.g., isoprenaline).
    • Measurement of basal and stimulated cyclic AMP levels.
    • Evaluation of beta-adrenergic receptor number and affinity.

    Main Results:

    • PMA treatment did not alter basal cyclic AMP levels.
    • PMA treatment did not change the number or affinity of epidermal beta-receptors.
    • PMA sharply inhibited cyclic AMP accumulation in response to isoprenaline injection.
    • Evidence suggests PMA uncouples epidermal beta-receptors from adenylate cyclase.

    Conclusions:

    • PMA's inhibition of epidermal responsiveness to catecholamines is mediated by uncoupling beta-adrenergic receptors from adenylate cyclase.
    • This uncoupling occurs independently of changes in basal cyclic AMP levels or receptor binding characteristics.

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