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    Low concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine expression in cultured astrocytes

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    Authors
    DeVito, William J.
    Stone, Scott
    Mori, Kouki
    UMass Chan Affiliations
    Division of Endocrinology
    Document Type
    Journal Article
    Publication Date
    1997-03-01
    Keywords
    Animals
    Astrocytes
    Cells, Cultured
    Cytokines
    Ethanol
    Female
    Mitosis
    Osmolar Concentration
    Pregnancy
    Prenatal Exposure Delayed Effects
    Prolactin
    Rats
    Thymidine
    Tumor Necrosis Factor-alpha
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://doi.org/10.1210/en.138.3.922
    Abstract
    Whereas the immunosuppressive effects of chronic alcohol use have been well documented, little is known about the effect of ethanol on the neuroimmune response. We previously demonstrated that PRL is a potent mitogen and induces the expression of several inflammatory cytokines, including tumor necrosis factor-alpha (TNF alpha) in cultured rat astrocytes. The aim of this study was to examine the effects of ethanol on PRL-induced mitogenesis and TNF alpha expression in cultured rat astrocytes. We found that low concentrations of ethanol blocked PRL-induced increases in [3H]thymidine incorporation and TNF alpha levels. In contrast, ethanol had no effect on platelet-derived growth factor- or fibroblast growth factor-induced increases in [3H]thymidine incorporation. Radioligand binding analysis revealed that ethanol did not effect PRL receptor binding. We also examined the effect of prenatal alcohol exposure (PAE) on PRL-induced mitogenesis and cytokine expression. PAE during the last 5 days of gestation blunted the PRL-induced increase in [3H]thymidine incorporation and TNF alpha levels in cells grown in the absence of ethanol in the culture medium. Addition of ethanol to primary PAE astrocyte cultures resulted in a modest increase in basal [3H]thymidine incorporation, but completely blocked the PRL-induced increase in [3H]thymidine incorporation and TNF alpha levels. In contrast, platelet-derived growth factor- and serum (10%)-induced increases in [3H]thymidine incorporation remained intact. Together, these data indicate that ethanol blocks PRL-induced mitogenesis and the expression of TNF alpha in cultured rat astrocytes and are consistent with the possible inhibition of the astrocytic response by ethanol in vivo.
    Source

    Endocrinology. 1997 Mar;138(3):922-8.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/42152
    PubMed ID
    9048591
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