Activation of the CAMP Cascade Inhibits an Early Event Involved in Murine Macrophage Ia Expression
Autor(a) principal: | |
---|---|
Data de Publicação: | 1990 |
Outros Autores: | , , , , , |
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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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 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
status_str |
publishedVersion |
format |
article |
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 |
url |
http://hdl.handle.net/123456789/202 https://repositorio.ucb.br:9443/jspui/handle/123456789/7425 |
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eng |
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eng |
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openAccess |
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UCB |
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UCB |
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Repositório Institucional da UCB |
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Repositório Institucional da UCB |
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