Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression

Detalhes bibliográficos
Autor(a) principal: Figueiredo, Florêncio
Data de Publicação: 1990
Outros Autores: Uhing, Ronald J., Kenji, Okonogi, Gettys, Tom W., Johnson, Stewart P., Adams, Dolph O, Prpic, Verônica
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UCB
Texto Completo: http://hdl.handle.net/123456789/202
https://repositorio.ucb.br:9443/jspui/handle/123456789/7425
Resumo: The ability of interferon-gamma (IFN gamma) to increase class II major histocompatibility complex (class II MHC) gene products in murine macrophages involves activation of Na+/H+ exchange (Prpic V., Yu, S. F., Figueiredo, F., Hollenbach, P. W., Gawdi, G., Herman, B., Uhing, R. J., and Adams, D. O. (1989) Science 244, 469-471). The ability of IFN gamma to increase class II MHC gene product expression is inhibited by a variety of agents. In the present studies, the involvement of cAMP-dependent protein kinase in modulating IFN gamma-induced expression of MHC gene products and the mechanism of regulation were assessed in macrophages treated with agents which activated cAMP-dependent protein kinase by different molecular mechanisms. Prostaglandin E2 (PGE2) produced a rapid (within 30 s) dose-dependent elevation of cAMP which was paralleled by the activation of cAMP-dependent protein kinase. The elevation of cAMP by PGE2 was still evident at 1 h and maintained through a 4-h incubation. Concentrations of PGE2 which activated the protein kinase produced a dose-dependent inhibition of surface expression of I-A and transcription of class II MHC genes. Inhibition of IFN gamma-induced class II MHC gene product expression was also observed in macrophages treated with agents which activated cAMP-dependent protein kinase by postreceptor mechanisms. Dibutyryl-cAMP (0.01-1 mM), 25 microM forskolin, 0.1 micrograms/ml cholera toxin, and 3-isobutyl-1-methylxanthine (0.1-1 mM) each suppressed IFN gamma-induced cell surface I-A expression, class II MHC gene transcription, and 22Na+ influx. The results are consistent with the suggestion that activation of cAMP-dependent protein kinase regulates an early transductional event initiated by IFN gamma, perhaps Na+/H+ exchange, which is involved in regulating transcription of class II MHC genes and their subsequent expression.
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spelling Figueiredo, FlorêncioUhing, Ronald J.Kenji, OkonogiGettys, Tom W.Johnson, Stewart P.Adams, Dolph OPrpic, Verônica2016-10-10T03:51:26Z2016-10-10T03:51:26Z1990FIGUEIREDO, Florêncio. et al. Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression. The Journal of Biological Chemistry, v. 165, n. 21, p. 12317-12323, 1990.219258http://hdl.handle.net/123456789/202https://repositorio.ucb.br:9443/jspui/handle/123456789/7425The ability of interferon-gamma (IFN gamma) to increase class II major histocompatibility complex (class II MHC) gene products in murine macrophages involves activation of Na+/H+ exchange (Prpic V., Yu, S. F., Figueiredo, F., Hollenbach, P. W., Gawdi, G., Herman, B., Uhing, R. J., and Adams, D. O. (1989) Science 244, 469-471). The ability of IFN gamma to increase class II MHC gene product expression is inhibited by a variety of agents. In the present studies, the involvement of cAMP-dependent protein kinase in modulating IFN gamma-induced expression of MHC gene products and the mechanism of regulation were assessed in macrophages treated with agents which activated cAMP-dependent protein kinase by different molecular mechanisms. Prostaglandin E2 (PGE2) produced a rapid (within 30 s) dose-dependent elevation of cAMP which was paralleled by the activation of cAMP-dependent protein kinase. The elevation of cAMP by PGE2 was still evident at 1 h and maintained through a 4-h incubation. Concentrations of PGE2 which activated the protein kinase produced a dose-dependent inhibition of surface expression of I-A and transcription of class II MHC genes. Inhibition of IFN gamma-induced class II MHC gene product expression was also observed in macrophages treated with agents which activated cAMP-dependent protein kinase by postreceptor mechanisms. Dibutyryl-cAMP (0.01-1 mM), 25 microM forskolin, 0.1 micrograms/ml cholera toxin, and 3-isobutyl-1-methylxanthine (0.1-1 mM) each suppressed IFN gamma-induced cell surface I-A expression, class II MHC gene transcription, and 22Na+ influx. The results are consistent with the suggestion that activation of cAMP-dependent protein kinase regulates an early transductional event initiated by IFN gamma, perhaps Na+/H+ exchange, which is involved in regulating transcription of class II MHC genes and their subsequent expression.Made available in DSpace on 2016-10-10T03:51:26Z (GMT). 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dc.title.pt_BR.fl_str_mv Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
title Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
spellingShingle Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
Figueiredo, Florêncio
Ciências da saúde
Medicina
Patologia clínica
title_short Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
title_full Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
title_fullStr Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
title_full_unstemmed Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
title_sort Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
author Figueiredo, Florêncio
author_facet Figueiredo, Florêncio
Uhing, Ronald J.
Kenji, Okonogi
Gettys, Tom W.
Johnson, Stewart P.
Adams, Dolph O
Prpic, Verônica
author_role author
author2 Uhing, Ronald J.
Kenji, Okonogi
Gettys, Tom W.
Johnson, Stewart P.
Adams, Dolph O
Prpic, Verônica
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Figueiredo, Florêncio
Uhing, Ronald J.
Kenji, Okonogi
Gettys, Tom W.
Johnson, Stewart P.
Adams, Dolph O
Prpic, Verônica
dc.subject.por.fl_str_mv Ciências da saúde
Medicina
Patologia clínica
topic Ciências da saúde
Medicina
Patologia clínica
dc.description.abstract.por.fl_txt_mv The ability of interferon-gamma (IFN gamma) to increase class II major histocompatibility complex (class II MHC) gene products in murine macrophages involves activation of Na+/H+ exchange (Prpic V., Yu, S. F., Figueiredo, F., Hollenbach, P. W., Gawdi, G., Herman, B., Uhing, R. J., and Adams, D. O. (1989) Science 244, 469-471). The ability of IFN gamma to increase class II MHC gene product expression is inhibited by a variety of agents. In the present studies, the involvement of cAMP-dependent protein kinase in modulating IFN gamma-induced expression of MHC gene products and the mechanism of regulation were assessed in macrophages treated with agents which activated cAMP-dependent protein kinase by different molecular mechanisms. Prostaglandin E2 (PGE2) produced a rapid (within 30 s) dose-dependent elevation of cAMP which was paralleled by the activation of cAMP-dependent protein kinase. The elevation of cAMP by PGE2 was still evident at 1 h and maintained through a 4-h incubation. Concentrations of PGE2 which activated the protein kinase produced a dose-dependent inhibition of surface expression of I-A and transcription of class II MHC genes. Inhibition of IFN gamma-induced class II MHC gene product expression was also observed in macrophages treated with agents which activated cAMP-dependent protein kinase by postreceptor mechanisms. Dibutyryl-cAMP (0.01-1 mM), 25 microM forskolin, 0.1 micrograms/ml cholera toxin, and 3-isobutyl-1-methylxanthine (0.1-1 mM) each suppressed IFN gamma-induced cell surface I-A expression, class II MHC gene transcription, and 22Na+ influx. The results are consistent with the suggestion that activation of cAMP-dependent protein kinase regulates an early transductional event initiated by IFN gamma, perhaps Na+/H+ exchange, which is involved in regulating transcription of class II MHC genes and their subsequent expression.
dc.description.version.pt_BR.fl_txt_mv Sim
dc.description.status.pt_BR.fl_txt_mv Publicado
description The ability of interferon-gamma (IFN gamma) to increase class II major histocompatibility complex (class II MHC) gene products in murine macrophages involves activation of Na+/H+ exchange (Prpic V., Yu, S. F., Figueiredo, F., Hollenbach, P. W., Gawdi, G., Herman, B., Uhing, R. J., and Adams, D. O. (1989) Science 244, 469-471). The ability of IFN gamma to increase class II MHC gene product expression is inhibited by a variety of agents. In the present studies, the involvement of cAMP-dependent protein kinase in modulating IFN gamma-induced expression of MHC gene products and the mechanism of regulation were assessed in macrophages treated with agents which activated cAMP-dependent protein kinase by different molecular mechanisms. Prostaglandin E2 (PGE2) produced a rapid (within 30 s) dose-dependent elevation of cAMP which was paralleled by the activation of cAMP-dependent protein kinase. The elevation of cAMP by PGE2 was still evident at 1 h and maintained through a 4-h incubation. Concentrations of PGE2 which activated the protein kinase produced a dose-dependent inhibition of surface expression of I-A and transcription of class II MHC genes. Inhibition of IFN gamma-induced class II MHC gene product expression was also observed in macrophages treated with agents which activated cAMP-dependent protein kinase by postreceptor mechanisms. Dibutyryl-cAMP (0.01-1 mM), 25 microM forskolin, 0.1 micrograms/ml cholera toxin, and 3-isobutyl-1-methylxanthine (0.1-1 mM) each suppressed IFN gamma-induced cell surface I-A expression, class II MHC gene transcription, and 22Na+ influx. The results are consistent with the suggestion that activation of cAMP-dependent protein kinase regulates an early transductional event initiated by IFN gamma, perhaps Na+/H+ exchange, which is involved in regulating transcription of class II MHC genes and their subsequent expression.
publishDate 1990
dc.date.issued.fl_str_mv 1990
dc.date.accessioned.fl_str_mv 2016-10-10T03:51:26Z
dc.date.available.fl_str_mv 2016-10-10T03:51:26Z
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dc.identifier.citation.fl_str_mv FIGUEIREDO, Florêncio. et al. Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression. The Journal of Biological Chemistry, v. 165, n. 21, p. 12317-12323, 1990.
dc.identifier.uri.fl_str_mv http://hdl.handle.net/123456789/202
https://repositorio.ucb.br:9443/jspui/handle/123456789/7425
dc.identifier.issn.none.fl_str_mv 219258
identifier_str_mv FIGUEIREDO, Florêncio. et al. Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression. The Journal of Biological Chemistry, v. 165, n. 21, p. 12317-12323, 1990.
219258
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