V. Ramkumar et al., DEXAMETHASONE UP-REGULATES A(3) ADENOSINE RECEPTORS IN RAT BASOPHILICLEUKEMIA (RBL-2H3) CELLS, The Journal of immunology, 154(10), 1995, pp. 5436-5443
The cross-linking of surface IgE receptors by multi-functional Ags pro
motes the degranulation of mast cells. Previous studies have indicated
that the nucleoside adenosine potentiates this response by activating
putative A(3) adenosine receptors (AR) coupled to phospholipase C in
mast cells or their cultured analogues, rat basophilic leukemia (RBL-2
H3) cells. Moreover, it has been shown that exposure of RBL-2H3 cells
to dexamethasone attenuated antigen-mediated mast cell degranulation,
but potentiated the response elicited by adenosine. To determine wheth
er the A(3)AR is a potential site of action of dexamethasone, we have
assessed the status of these receptors in RBL-2H3 cells treated with a
nd without dexamethasone. Treatment with dexamethasone (100 nM) for 24
h resulted in an increase in the number of A(3)AR to 217 +/- 50% of c
ontrol. The increased receptor expression was both time- and concentra
tion-dependent, with optimal increases observed following 16 h of trea
tment and using 100 nM of dexamethasone. No increase in the level of t
he A(2a)AR was detectable following dexamethasone treatment. Northern
blotting studies indicated a 2.7 +/- 0.3-fold increase in A(3)AR mRNA
in RBL-2H3 cells treated with dexamethasone for 24 h. Dexamethasone al
so increased the expression of G protein alpha(i2), alpha(i3), alpha(s
), and beta subunits by two- to threefold. Activation of the A(3)AR by
aminophenylethyladenosine (APNEA) following dexamethasone treatment e
nhanced the production of inositol phosphates and the mobilization of
intracellular Ca2+ From these data, it is concluded that dexamethasone
increases the expression of both A(3)AR and G proteins in RBL-2H3 cel
ls which contributes to the enhanced response to adenosine.