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Recombinant human interleukin‐1 inhibits the induction by dexamethasone of alkaline phosphatase activity in murine capillary endothelial cells
Author(s) -
Mulkins Mary A.,
Allison Anthony C.
Publication year - 1987
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041330315
Subject(s) - alkaline phosphatase , dexamethasone , glucocorticoid receptor , glucocorticoid , antagonism , receptor , endocrinology , medicine , chemistry , biology , biochemistry , enzyme
A mutual antagonism exists between interleukin‐1s (IL‐1s) as pro‐inflammatory and glucocorticoids as anti‐inflammatory mediators. This report examines the effects of IL‐1 on the induction by dexamethasone of alkaline phosphatase in LEII murine endothelial cells. Dexamethasone increases the specific activity of alkaline phosphatase in a time‐ and dose‐dependent fashion (maximum 14‐fold induction at 10 −6 M, IC 50 = 10 −8 M), and this induction can be completely inhibited by simultaneous incubation with picomolar concentrations of recombinant human IL‐1α or IL‐1β. This IL‐1‐mediated antagonism of dexamethasone activity is not due to a down‐regulation of glucocorticoid receptors in the cell line used, because the number of receptors and their affinity for dexamethasone is unchanged in IL‐1‐treated cells. However, induction of alkaline phosphatase by dexamethasone in LEII cells is receptor‐mediated, since it can also be inhibited by glucocorticoid‐receptor antagonists.