Glucocorticoid receptors and cortico‐sensitivity in a human clonal monocytic cell line, CM‐SM

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Abstract
CM‐SM is a clonal line of human precursor mononuclear phagocytes inducible to macrophage differentiation in response to the tumor promoter phorbol ester 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA). Untreated CM‐SM cells contain single class, high‐affinity (KD = 4.0 × 10−9 M) glucocorticoid‐specific receptor sites (∼60,000 per cell), as measured by a whole cell assay, at 37°C, using [3H]triamcinolone acetonide (TA). Exposure of CM‐SM to dexamethasone (DEX) produced a progressive, dose‐ and time‐related series of changes in CM‐SM cell growth, saturation density, morphology, and functional properties, with half‐maximal effects at about 10−9 M for DEX. TA‐receptor sites rapidly decreased (about 70%) after DEX treatment, without any apparent change in steroid specificity and affinity. After 5 days in culture with a saturating concentration (3.6 × 10−8 M) of hormone, the cells reached a saturation density of about 9.0 × 106 viable cells/ml (about 4.0 × 106 viable cells/ml in the controls), while the modal volume of the resulting cell population was approximately 60%, as compared to the volume of untreated cells. DEX‐treated cells appeared less differentiated than controls, as assessed by combined morphologic, antigenic, and cytoenzymatic analyses. DEX almost completely inhibited TPA activation of the following macrophage functions: adherency to the culture plate, expression of lysosomal enzymes, Fc and C3 receptors, and stimulation of phagocytosis. After removal of DEX, the cells, within a few passages, returned to a state apparently identical to the untreated controls and could be induced to macrophage differentiation in response to TPA.