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Differential effect of dexamethasone on the regulation of phospholipase A 2 and prostanoid synthesis in undifferentiated and phorbolester‐differentiated U937 cells
Author(s) -
Koehler L.,
Hass R.,
GoppeltStruebe M.,
Kaever V.,
Resch K.
Publication year - 1989
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240400315
Subject(s) - u937 cell , phospholipase a2 , arachidonic acid , prostanoid , monocyte , cell culture , cellular differentiation , prostaglandin , chemistry , endocrinology , medicine , biology , biochemistry , microbiology and biotechnology , enzyme , immunology , apoptosis , genetics , gene
The human undifferentiated histiocytic cell‐line U937 can be induced to differentiate by incubation with 12‐0‐tetradecanoylphorbol‐13‐acetate (TPA) into macrophage‐like cells. Dexamethasone reduced the prostaglandin production in TPA‐differentiated U937 cells dose dependently, whereas undifferentiated U937 cells were dexamethasone insensitive. Concomitantly phospholipase A 2 , the enzyme liberating the prostaglandin precursor arachidonic acid, was inhibited by dexamethasone in TPA‐differentiated but not in undifferentiated U937 cells. The activity of lysophosphatide acyltransferase, the key enzyme of fatty acid reacylation into phospholipids, remained unchanged both in undifferentiated and TPA‐differentiated U937 cells. The data suggest that responsiveness to glucocorticoid‐dependent regulation of prostanoid synthesis is acquired by cells of the monocyte‐macrophage lineage late in differentiation.