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Indomethacin causes a simultaneous decrease of both prolactin binding and fluidity of mouse liver membranes.

R A Knazek, S C Liu, J R Dave

    Prostaglandins and Medicine
    |April 1, 1981
    PubMed
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    Indomethacin reduces prolactin receptors in mouse liver membranes, affecting membrane fluidity. Prolactin cannot overcome indomethacin

    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Biochemistry

    Background:

    • Prolactin is a key hormone regulating numerous physiological processes.
    • Prolactin receptors are crucial for mediating prolactin's effects.
    • The role of prostaglandins in prolactin receptor regulation is not fully understood.

    Purpose of the Study:

    • To investigate the effect of indomethacin on prolactin receptor expression and liver membrane fluidity.
    • To explore the potential involvement of the prostaglandin cascade in prolactin receptor induction.

    Main Methods:

    • Dose-dependent administration of indomethacin and prolactin to C3H mice.
    • Quantification of liver membrane prolactin receptors.
    • Assessment of membrane fluidity using fluorescence polarization with 1,6-diphenylhexatriene.

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    Main Results:

    • Indomethacin significantly suppressed prolactin receptor numbers in a dose-dependent manner.
    • Indomethacin decreased liver membrane fluidity.
    • Exogenous prolactin increased membrane fluidity but could not counteract indomethacin's effects on receptors or fluidity.

    Conclusions:

    • Indomethacin interferes with prolactin receptor expression, potentially via the prostaglandin cascade.
    • Prolactin receptor induction may involve alterations in membrane lipid bilayer fluidity.
    • Data suggest prolactin may induce its own receptor through prostaglandin-mediated mechanisms.