Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells

Autores
Mori Sequeiros, María de Las Mercedes; Cohen Sabban, Juan Manuel; Dattilo, Melina Andrea; Mele, Pablo Gustavo; Nudler, Silvana Iris; Mendez, Carlos Fernando; Maloberti, Paula Mariana; Paz, Cristina del Valle
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
MAPK phosphatases (MKP) downregulate the activity of mitogen-activated protein kinases (MAPK), such asERK1/2, and modulate the processes regulated by these kinases. ERK1/2 participate in a wide range of processesincluding tissue-specific hormone-stimulated steroidogenesis. H295R cells are a suitable model for the study ofhuman adrenal cortex functions, particularly steroid synthesis, and respond to angiotensin II (Ang II) triggeringERK1/2 phosphorylation in a transient fashion. MKP-3 dephosphorylates ERK1/2 and, as recently reported,forkhead box protein 1 (FOXO1). Here, we analyzed MKP-3 expression in H295R cells and its putative regulationby Ang II. Results showed the expression of MKP-3 full length (L) and a short splice variant (S), and the upregulationof both isoforms by Ang II. L and S messenger and protein levels increased 30 min after Ang II stimulationand declined over the next 3 h, a temporal frame compatible with ERK1/2 dephosphorylation. In addition, FOXO1activation is known to include its dephosphorylation and nuclear translocation. Therefore, we analyzed the effectof Ang II on FOXO1 modulation. Ang II induced FOXO1 transient phosphorylation and translocation and also theinduction of p21, a FOXO1-dependent gene, whereas MKP-3 knock-down reduced both FOXO1 translocation andp21 induction. These data suggest that, through MKP-3, Ang II counteracts its own effects on ERK1/2 activity andalso triggers the activation of FOXO-1 and the induction of cell cycle inhibitor p21. Taken together, the currentfindings reveal the participation of MKP-3 not only in turn?off but also in turn-on signals which control importantcellular processes.
Fil: Mori Sequeiros, María de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Cohen Sabban, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Dattilo, Melina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mele, Pablo Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Nudler, Silvana Iris. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mendez, Carlos Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Paz, Cristina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Materia
ANGIOTENSIN II
MAP KINASE PHOSPHATASE 3
FOXO1
P21
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/104958
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/104958
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cellsMori Sequeiros, María de Las MercedesCohen Sabban, Juan ManuelDattilo, Melina AndreaMele, Pablo GustavoNudler, Silvana IrisMendez, Carlos FernandoMaloberti, Paula MarianaPaz, Cristina del ValleANGIOTENSIN IIMAP KINASE PHOSPHATASE 3FOXO1P21https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1MAPK phosphatases (MKP) downregulate the activity of mitogen-activated protein kinases (MAPK), such asERK1/2, and modulate the processes regulated by these kinases. ERK1/2 participate in a wide range of processesincluding tissue-specific hormone-stimulated steroidogenesis. H295R cells are a suitable model for the study ofhuman adrenal cortex functions, particularly steroid synthesis, and respond to angiotensin II (Ang II) triggeringERK1/2 phosphorylation in a transient fashion. MKP-3 dephosphorylates ERK1/2 and, as recently reported,forkhead box protein 1 (FOXO1). Here, we analyzed MKP-3 expression in H295R cells and its putative regulationby Ang II. Results showed the expression of MKP-3 full length (L) and a short splice variant (S), and the upregulationof both isoforms by Ang II. L and S messenger and protein levels increased 30 min after Ang II stimulationand declined over the next 3 h, a temporal frame compatible with ERK1/2 dephosphorylation. In addition, FOXO1activation is known to include its dephosphorylation and nuclear translocation. Therefore, we analyzed the effectof Ang II on FOXO1 modulation. Ang II induced FOXO1 transient phosphorylation and translocation and also theinduction of p21, a FOXO1-dependent gene, whereas MKP-3 knock-down reduced both FOXO1 translocation andp21 induction. These data suggest that, through MKP-3, Ang II counteracts its own effects on ERK1/2 activity andalso triggers the activation of FOXO-1 and the induction of cell cycle inhibitor p21. Taken together, the currentfindings reveal the participation of MKP-3 not only in turn?off but also in turn-on signals which control importantcellular processes.Fil: Mori Sequeiros, María de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Cohen Sabban, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Dattilo, Melina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Mele, Pablo Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Nudler, Silvana Iris. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Mendez, Carlos Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Paz, Cristina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaCell Press2020-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/104958Mori Sequeiros, María de Las Mercedes; Cohen Sabban, Juan Manuel; Dattilo, Melina Andrea; Mele, Pablo Gustavo; Nudler, Silvana Iris; et al.; Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells; Cell Press; Heliyon; 6; 3; 3-2020; 1-82405-8440CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.heliyon.2020.e03519info:eu-repo/semantics/altIdentifier/url/https://www.cell.com/heliyon/pdf/S2405-8440(20)30364-9.pdf?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2405844020303649%3Fshowall%3Dtrueinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066232/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:25:16Zoai:ri.conicet.gov.ar:11336/104958instacron: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:34982025-10-22 11:25:17.022CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
title Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
spellingShingle Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
Mori Sequeiros, María de Las Mercedes
ANGIOTENSIN II
MAP KINASE PHOSPHATASE 3
FOXO1
P21
title_short Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
title_full Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
title_fullStr Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
title_full_unstemmed Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
title_sort Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells
dc.creator.none.fl_str_mv Mori Sequeiros, María de Las Mercedes
Cohen Sabban, Juan Manuel
Dattilo, Melina Andrea
Mele, Pablo Gustavo
Nudler, Silvana Iris
Mendez, Carlos Fernando
Maloberti, Paula Mariana
Paz, Cristina del Valle
author Mori Sequeiros, María de Las Mercedes
author_facet Mori Sequeiros, María de Las Mercedes
Cohen Sabban, Juan Manuel
Dattilo, Melina Andrea
Mele, Pablo Gustavo
Nudler, Silvana Iris
Mendez, Carlos Fernando
Maloberti, Paula Mariana
Paz, Cristina del Valle
author_role author
author2 Cohen Sabban, Juan Manuel
Dattilo, Melina Andrea
Mele, Pablo Gustavo
Nudler, Silvana Iris
Mendez, Carlos Fernando
Maloberti, Paula Mariana
Paz, Cristina del Valle
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANGIOTENSIN II
MAP KINASE PHOSPHATASE 3
FOXO1
P21
topic ANGIOTENSIN II
MAP KINASE PHOSPHATASE 3
FOXO1
P21
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv MAPK phosphatases (MKP) downregulate the activity of mitogen-activated protein kinases (MAPK), such asERK1/2, and modulate the processes regulated by these kinases. ERK1/2 participate in a wide range of processesincluding tissue-specific hormone-stimulated steroidogenesis. H295R cells are a suitable model for the study ofhuman adrenal cortex functions, particularly steroid synthesis, and respond to angiotensin II (Ang II) triggeringERK1/2 phosphorylation in a transient fashion. MKP-3 dephosphorylates ERK1/2 and, as recently reported,forkhead box protein 1 (FOXO1). Here, we analyzed MKP-3 expression in H295R cells and its putative regulationby Ang II. Results showed the expression of MKP-3 full length (L) and a short splice variant (S), and the upregulationof both isoforms by Ang II. L and S messenger and protein levels increased 30 min after Ang II stimulationand declined over the next 3 h, a temporal frame compatible with ERK1/2 dephosphorylation. In addition, FOXO1activation is known to include its dephosphorylation and nuclear translocation. Therefore, we analyzed the effectof Ang II on FOXO1 modulation. Ang II induced FOXO1 transient phosphorylation and translocation and also theinduction of p21, a FOXO1-dependent gene, whereas MKP-3 knock-down reduced both FOXO1 translocation andp21 induction. These data suggest that, through MKP-3, Ang II counteracts its own effects on ERK1/2 activity andalso triggers the activation of FOXO-1 and the induction of cell cycle inhibitor p21. Taken together, the currentfindings reveal the participation of MKP-3 not only in turn?off but also in turn-on signals which control importantcellular processes.
Fil: Mori Sequeiros, María de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Cohen Sabban, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Dattilo, Melina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mele, Pablo Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Nudler, Silvana Iris. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Mendez, Carlos Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Paz, Cristina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
description MAPK phosphatases (MKP) downregulate the activity of mitogen-activated protein kinases (MAPK), such asERK1/2, and modulate the processes regulated by these kinases. ERK1/2 participate in a wide range of processesincluding tissue-specific hormone-stimulated steroidogenesis. H295R cells are a suitable model for the study ofhuman adrenal cortex functions, particularly steroid synthesis, and respond to angiotensin II (Ang II) triggeringERK1/2 phosphorylation in a transient fashion. MKP-3 dephosphorylates ERK1/2 and, as recently reported,forkhead box protein 1 (FOXO1). Here, we analyzed MKP-3 expression in H295R cells and its putative regulationby Ang II. Results showed the expression of MKP-3 full length (L) and a short splice variant (S), and the upregulationof both isoforms by Ang II. L and S messenger and protein levels increased 30 min after Ang II stimulationand declined over the next 3 h, a temporal frame compatible with ERK1/2 dephosphorylation. In addition, FOXO1activation is known to include its dephosphorylation and nuclear translocation. Therefore, we analyzed the effectof Ang II on FOXO1 modulation. Ang II induced FOXO1 transient phosphorylation and translocation and also theinduction of p21, a FOXO1-dependent gene, whereas MKP-3 knock-down reduced both FOXO1 translocation andp21 induction. These data suggest that, through MKP-3, Ang II counteracts its own effects on ERK1/2 activity andalso triggers the activation of FOXO-1 and the induction of cell cycle inhibitor p21. Taken together, the currentfindings reveal the participation of MKP-3 not only in turn?off but also in turn-on signals which control importantcellular processes.
publishDate 2020
dc.date.none.fl_str_mv 2020-03
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/11336/104958
Mori Sequeiros, María de Las Mercedes; Cohen Sabban, Juan Manuel; Dattilo, Melina Andrea; Mele, Pablo Gustavo; Nudler, Silvana Iris; et al.; Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells; Cell Press; Heliyon; 6; 3; 3-2020; 1-8
2405-8440
CONICET Digital
CONICET
url http://hdl.handle.net/11336/104958
identifier_str_mv Mori Sequeiros, María de Las Mercedes; Cohen Sabban, Juan Manuel; Dattilo, Melina Andrea; Mele, Pablo Gustavo; Nudler, Silvana Iris; et al.; Angiotensin II-upregulated MAP kinase phosphatase-3 modulates FOXO1 and p21 in adrenocortical H295R cells; Cell Press; Heliyon; 6; 3; 3-2020; 1-8
2405-8440
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.heliyon.2020.e03519
info:eu-repo/semantics/altIdentifier/url/https://www.cell.com/heliyon/pdf/S2405-8440(20)30364-9.pdf?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2405844020303649%3Fshowall%3Dtrue
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066232/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Cell Press
publisher.none.fl_str_mv Cell Press
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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