Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.

Autores
Albertoni Borghese, Maria Florencia; Bettini, Layne M.; Nitta, Carlos H.; de Frutos, Sergio; Majowicz, Mónica; González Bosc, Laura Veronica
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background/aims: We have previously shown that aquaporin-2 (AQP2) is down-regulated in the renal medulla of rats made hypertensive by chronic inhibition of nitric oxide synthase (NOS). It has been shown that AQP2 expression is regulated by the calcineurin/ nuclear factor of activated T cells (NFATc). Nitric oxide (NO) regulates the activity of NFATc via c-Jun-N-terminal kinase 2 (JNK2). Therefore, we hypothesized that increases in NO enhance NFATc-mediated up-regulation of AQP2 promoter activity. Methods: AQP2 mRNA and protein expression were detected in mouse renal papilla. AQP2-promoter-luciferase reporter and NFAT-luciferase reporter transfected MDCK cells were used to determine AQP2 promoter activity and NFATc activity, respectively. Cells were incubated with classic activators and inhibitors of NFATc and NO pathway. Results: Our results demonstrate that both Ca2+ and NO have a synergistic effect in increasing AQP2 mRNA and protein in mouse papilla, and in activating the AQP2 promoter in kidney-derived cells. In addition, NO enhances Ca2+-induced NFATc activation. The underlying mechanism involves increased NFATc nuclear import and decreased export via PKG-mediated inhibition of JNK1/2. Conclusions: This is the first study defining novel regulatory roles for NO and NFATc in the control of AQP2 expression, which is an important renal protein.
Fil: Albertoni Borghese, Maria Florencia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Bettini, Layne M.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: Nitta, Carlos H.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: de Frutos, Sergio. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: Majowicz, Mónica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: González Bosc, Laura Veronica. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Materia
Aquaporin 2
Nitric Oxide
Nfatc
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/12873
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/12873
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.Albertoni Borghese, Maria FlorenciaBettini, Layne M.Nitta, Carlos H.de Frutos, SergioMajowicz, MónicaGonzález Bosc, Laura VeronicaAquaporin 2Nitric OxideNfatchttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Background/aims: We have previously shown that aquaporin-2 (AQP2) is down-regulated in the renal medulla of rats made hypertensive by chronic inhibition of nitric oxide synthase (NOS). It has been shown that AQP2 expression is regulated by the calcineurin/ nuclear factor of activated T cells (NFATc). Nitric oxide (NO) regulates the activity of NFATc via c-Jun-N-terminal kinase 2 (JNK2). Therefore, we hypothesized that increases in NO enhance NFATc-mediated up-regulation of AQP2 promoter activity. Methods: AQP2 mRNA and protein expression were detected in mouse renal papilla. AQP2-promoter-luciferase reporter and NFAT-luciferase reporter transfected MDCK cells were used to determine AQP2 promoter activity and NFATc activity, respectively. Cells were incubated with classic activators and inhibitors of NFATc and NO pathway. Results: Our results demonstrate that both Ca2+ and NO have a synergistic effect in increasing AQP2 mRNA and protein in mouse papilla, and in activating the AQP2 promoter in kidney-derived cells. In addition, NO enhances Ca2+-induced NFATc activation. The underlying mechanism involves increased NFATc nuclear import and decreased export via PKG-mediated inhibition of JNK1/2. Conclusions: This is the first study defining novel regulatory roles for NO and NFATc in the control of AQP2 expression, which is an important renal protein.Fil: Albertoni Borghese, Maria Florencia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Bettini, Layne M.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados UnidosFil: Nitta, Carlos H.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados UnidosFil: de Frutos, Sergio. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados UnidosFil: Majowicz, Mónica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: González Bosc, Laura Veronica. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados UnidosKarger2011-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/12873Albertoni Borghese, Maria Florencia; Bettini, Layne M.; Nitta, Carlos H.; de Frutos, Sergio; Majowicz, Mónica; et al.; Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.; Karger; Nephron EXTRA; 1; 1; 10-2011; 124-1381664-5529enginfo:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/333066info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290856/info:eu-repo/semantics/altIdentifier/doi/10.1159/000333066info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:20:39Zoai:ri.conicet.gov.ar:11336/12873instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:20:39.421CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
title Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
spellingShingle Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
Albertoni Borghese, Maria Florencia
Aquaporin 2
Nitric Oxide
Nfatc
title_short Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
title_full Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
title_fullStr Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
title_full_unstemmed Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
title_sort Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.
dc.creator.none.fl_str_mv Albertoni Borghese, Maria Florencia
Bettini, Layne M.
Nitta, Carlos H.
de Frutos, Sergio
Majowicz, Mónica
González Bosc, Laura Veronica
author Albertoni Borghese, Maria Florencia
author_facet Albertoni Borghese, Maria Florencia
Bettini, Layne M.
Nitta, Carlos H.
de Frutos, Sergio
Majowicz, Mónica
González Bosc, Laura Veronica
author_role author
author2 Bettini, Layne M.
Nitta, Carlos H.
de Frutos, Sergio
Majowicz, Mónica
González Bosc, Laura Veronica
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Aquaporin 2
Nitric Oxide
Nfatc
topic Aquaporin 2
Nitric Oxide
Nfatc
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Background/aims: We have previously shown that aquaporin-2 (AQP2) is down-regulated in the renal medulla of rats made hypertensive by chronic inhibition of nitric oxide synthase (NOS). It has been shown that AQP2 expression is regulated by the calcineurin/ nuclear factor of activated T cells (NFATc). Nitric oxide (NO) regulates the activity of NFATc via c-Jun-N-terminal kinase 2 (JNK2). Therefore, we hypothesized that increases in NO enhance NFATc-mediated up-regulation of AQP2 promoter activity. Methods: AQP2 mRNA and protein expression were detected in mouse renal papilla. AQP2-promoter-luciferase reporter and NFAT-luciferase reporter transfected MDCK cells were used to determine AQP2 promoter activity and NFATc activity, respectively. Cells were incubated with classic activators and inhibitors of NFATc and NO pathway. Results: Our results demonstrate that both Ca2+ and NO have a synergistic effect in increasing AQP2 mRNA and protein in mouse papilla, and in activating the AQP2 promoter in kidney-derived cells. In addition, NO enhances Ca2+-induced NFATc activation. The underlying mechanism involves increased NFATc nuclear import and decreased export via PKG-mediated inhibition of JNK1/2. Conclusions: This is the first study defining novel regulatory roles for NO and NFATc in the control of AQP2 expression, which is an important renal protein.
Fil: Albertoni Borghese, Maria Florencia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Bettini, Layne M.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: Nitta, Carlos H.. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: de Frutos, Sergio. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
Fil: Majowicz, Mónica. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: González Bosc, Laura Veronica. University Of New Mexico. School Of Medicine. Departament Of Cell Biology And Phisiology; Estados Unidos
description Background/aims: We have previously shown that aquaporin-2 (AQP2) is down-regulated in the renal medulla of rats made hypertensive by chronic inhibition of nitric oxide synthase (NOS). It has been shown that AQP2 expression is regulated by the calcineurin/ nuclear factor of activated T cells (NFATc). Nitric oxide (NO) regulates the activity of NFATc via c-Jun-N-terminal kinase 2 (JNK2). Therefore, we hypothesized that increases in NO enhance NFATc-mediated up-regulation of AQP2 promoter activity. Methods: AQP2 mRNA and protein expression were detected in mouse renal papilla. AQP2-promoter-luciferase reporter and NFAT-luciferase reporter transfected MDCK cells were used to determine AQP2 promoter activity and NFATc activity, respectively. Cells were incubated with classic activators and inhibitors of NFATc and NO pathway. Results: Our results demonstrate that both Ca2+ and NO have a synergistic effect in increasing AQP2 mRNA and protein in mouse papilla, and in activating the AQP2 promoter in kidney-derived cells. In addition, NO enhances Ca2+-induced NFATc activation. The underlying mechanism involves increased NFATc nuclear import and decreased export via PKG-mediated inhibition of JNK1/2. Conclusions: This is the first study defining novel regulatory roles for NO and NFATc in the control of AQP2 expression, which is an important renal protein.
publishDate 2011
dc.date.none.fl_str_mv 2011-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/12873
Albertoni Borghese, Maria Florencia; Bettini, Layne M.; Nitta, Carlos H.; de Frutos, Sergio; Majowicz, Mónica; et al.; Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.; Karger; Nephron EXTRA; 1; 1; 10-2011; 124-138
1664-5529
url http://hdl.handle.net/11336/12873
identifier_str_mv Albertoni Borghese, Maria Florencia; Bettini, Layne M.; Nitta, Carlos H.; de Frutos, Sergio; Majowicz, Mónica; et al.; Aquaporin-2 Promoter Is Synergistically Regulated by Nitric Oxide and Nuclear Factor of Activated T Cells.; Karger; Nephron EXTRA; 1; 1; 10-2011; 124-138
1664-5529
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/333066
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290856/
info:eu-repo/semantics/altIdentifier/doi/10.1159/000333066
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Karger
publisher.none.fl_str_mv Karger
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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