Abstract
AbstractThe relationship between cytosolic glucocorticoid receptors and two different physiological responses produced by dexamethasone (DEX) was investigated in steroid-sensitive C6 glioma cells and newly-derived, steroid-resistant C6H cells. Cell density measurements showed that cell proliferation was suppressed in 7.6 μM DEX-treated C6 cultures relative to controls. Scanning electron microscopy revealed that DEX-treated C6 cells and their processes were flattened compared to control C6 cells. In contrast, DEX failed to produce a growth-inhibitory response and morphological alterations in C6H cultures. Whole cell assays for glucocorticoid receptors indicated that specific binding (cpm/mg protein) of [3H]DEX and [3H]triamcinolone acetonide was similar in C6 and C6H cells. Assays employing cell-free preparations also showed that C6 and C6H cells contained similar amounts of steroid binding to cytosolic receptor sites. Thus, the loss of two physiological responses to DEX action in C6H cells is due to some ...
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Schedule a callMore From: Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
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