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Institute of Biology and Experimental Medicine, National Research
Council of Argentina, Obligado 2490 (1428) Buenos Aires, Argentina
(C.S., A.G.M., A.B.),
School of Sciences, University of Buenos Aires,
Argentina (C.S.), and
School of Pharmacy and Biochemistry, University
of Buenos Aires, Junin 956 (1133) Buenos Aires, Argentina (C.D., A.B.,
B.L.L., E.R.)
We examined the effects of histamine and its agonists on the expression
of the c-fos and c-myc proto-oncogenes at
the transcriptional and translational levels in the human promonocytic
U937 cell line. Histamine transiently increased cAMP and
c-fos expression through H2 receptors.
Dibutyryl cAMP also increased c-fos mRNA and protein, and levels
remained elevated even after 12 hr of treatment. Dose-dependence studies using histamine and dimaprit showed that the EC50
values for cAMP production and c-fos increase were
similar, suggesting that cAMP might be involved in c-fos
induction via H2 receptors. Furthermore, studies carried
out using H7, a protein kinase A/protein kinase C inhibitor, blocked
c-fos induction, whereas no effect was observed with
bisindolylmaleimide, a specific protein kinase C inhibitor. No
modification of c-myc expression could be detected on
treatment with histamine or its analogues. Nevertheless, dibutyryl cAMP
induced a down-regulation of the levels of this proto-oncogene. In
addition, dibutyryl cAMP inhibited cell growth in a dose-dependent manner, whereas histamine failed to affect proliferation and
differentiation of U937 cells. Cells pretreated with dimaprit showed a
decrease in the cAMP response to subsequent addition of H2
agonists, whereas the cAMP response to prostaglandin E2
remained unaltered. This homologous mechanism of H2
receptor desensitization was time dependent. These results indicate
that histamine activates several mechanisms involved in the induction
of differentiation, such as cAMP and c-fos production,
but fails to promote differentiation of U937 cells, apparently due to
the rapid desensitization of H2 receptors.
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