Histamine modulates the expression of c-fos through cyclic AMP production via the H2 receptor in the human promonocytic cell line U937

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...

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Autor principal: Shayo, C.
Otros Autores: Davio, C., Brodsky, A., Mladovan, A.G, Legnazzi, B.L, Rivera, E., Baldi, A.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: American Society for Pharmacology and Experimental Therapy 1997
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024 7 |2 cas  |a 1 (5 isoquinolinesulfonyl) 2 methylpiperazine, 84477-87-2; bucladesine, 16980-89-5, 362-74-3; cyclic AMP, 60-92-4; dimaprit, 65119-89-3; histamine, 51-45-6, 56-92-8, 93443-21-1; prostaglandin E2, 363-24-6 
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100 1 |a Shayo, C. 
245 1 0 |a Histamine modulates the expression of c-fos through cyclic AMP production via the H2 receptor in the human promonocytic cell line U937 
260 |b American Society for Pharmacology and Experimental Therapy  |c 1997 
270 1 0 |m Baldi, A.; Biology/Experimental Medicine Inst., Obligado 2490 (1428), Buenos Aires, Argentina; email: abaldi@proteus.dna.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a 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.  |l eng 
593 |a Inst. of Biol. and Exp. Medicine, Natl. Research Council of Argentina, Obligado 2490, (1428) Buenos Aires, Argentina 
593 |a School of Sciences, University of Buenos Aires, Argentina 
593 |a School of Pharmacy and Biochemistry, University of Buenos Aires, Junin 956, (1133) Buenos Aires, Argentina 
593 |a Inst. of Biol. and Exp. Medicine, Obligado 2490, (1428), Buenos Aires, Argentina 
690 1 0 |a 1 (5 ISOQUINOLINESULFONYL) 2 METHYLPIPERAZINE 
690 1 0 |a BISINDOLYLMALEIMIDE 
690 1 0 |a BUCLADESINE 
690 1 0 |a CYCLIC AMP 
690 1 0 |a CYCLIC AMP DEPENDENT PROTEIN KINASE INHIBITOR 
690 1 0 |a DIMAPRIT 
690 1 0 |a HISTAMINE 
690 1 0 |a HISTAMINE H2 RECEPTOR 
690 1 0 |a HISTAMINE H2 RECEPTOR ANTAGONIST 
690 1 0 |a MESSENGER RNA 
690 1 0 |a PROSTAGLANDIN E2 
690 1 0 |a PROTEIN C FOS 
690 1 0 |a PROTEIN KINASE C INHIBITOR 
690 1 0 |a ARTICLE 
690 1 0 |a CELL DIFFERENTIATION 
690 1 0 |a CELL GROWTH 
690 1 0 |a CHEMOTAXIS 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a HISTAMINE RELEASE 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a MONOCYTE 
690 1 0 |a ONCOGENE C FOS 
690 1 0 |a ONCOGENE C MYC 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a STEM CELL 
653 0 0 |a h 7, Sigma, United States 
700 1 |a Davio, C. 
700 1 |a Brodsky, A. 
700 1 |a Mladovan, A.G. 
700 1 |a Legnazzi, B.L. 
700 1 |a Rivera, E. 
700 1 |a Baldi, A. 
773 0 |d American Society for Pharmacology and Experimental Therapy, 1997  |g v. 51  |h pp. 983-990  |k n. 6  |p MOL. PHARMACOL.  |x 0026895X  |t Molecular Pharmacology 
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