In the cloned rat thymic endocrine epithelial cell line TEA3A1, treatment with dexamethasone leads to decreased levels of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2. Dexamethasone treatment also leads to a decrease of both calcium-dependent and calcium-independent phospholipase A2 activity measured in a cell-free assay. Dexamethasone-treated cells also have increased levels of lipocortin-I, a putative modulator of phospholipase A2 activity. The property of calcium-dependent binding of lipocortin to the particulate fraction was used to prepare cytosolic and particulate subcellular fractions which contained phospholiphase A2 activity but no lipocortin-I. Dexamethasone decreased phospholipase A2 activity in both cytosolic and particulate fractions even in the absence of lipocortin, suggesting the presence of a lipocortin-independent mechanism.

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