AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2

Autores
Rivarola, Valeria; Di Giusto, Gisela; Christensen, María José; Ford, Paula; Capurro, Claudia Graciela
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
We have previously shown in renal cells that expression of the water channel Aquaporin 2 (AQP2) increases the rate of cell proliferation by shortening the transit time through the S and G2/M phases of the cell cycle. This acceleration is due, at least in part; to a down-regulation of regulatory volume decrease (RVD) mechanisms when volume needs to be increased in order to proceed into the S phase. We hypothesize that in order to augment cell volume, RVD mechanisms may be overtaken by regulatory volume increase mechanisms (RVI). In this study, we investigated if the isoform 2 of the Na+/H+ exchanger (NHE2), the main ion transporter involved in RVI responses, contributed to the AQP2-increased renal cell proliferation. Two cortical collecting duct cell lines were used: WT-RCCD1 (not expressing AQPs) and AQP2-RCCD1 (transfected with AQP2). We here demonstrate, for the first time, that AQP2-expressing cells present both higher intracellular pH and higher NHE2 protein expression than WT-RCCD1 cells. In AQP2-expresing cells NHE2 inhibition decreased cell proliferation and delayed cell cycle progression by slowing S and G2/M phases. We also observed that only in AQP2-expressing cells a NHE2-dependent RVI response was activated in the S phase. These observations suggest that the AQP2-increased proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2. Therefore, we propose that the accelerated proliferation of AQP2-expressing cells requires a coordinated modulation of the RVD/RVI activity that contributes to cell volume changes during cell cycle progression.
Fil: Rivarola, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Di Giusto, Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Christensen, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Ford, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Capurro, Claudia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Materia
Aqp2
Cell Proliferation
Nhe2
Regulatory Volume Increase
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:11336/47443
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47443
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2Rivarola, ValeriaDi Giusto, GiselaChristensen, María JoséFord, PaulaCapurro, Claudia GracielaAqp2Cell ProliferationNhe2Regulatory Volume Increasehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3We have previously shown in renal cells that expression of the water channel Aquaporin 2 (AQP2) increases the rate of cell proliferation by shortening the transit time through the S and G2/M phases of the cell cycle. This acceleration is due, at least in part; to a down-regulation of regulatory volume decrease (RVD) mechanisms when volume needs to be increased in order to proceed into the S phase. We hypothesize that in order to augment cell volume, RVD mechanisms may be overtaken by regulatory volume increase mechanisms (RVI). In this study, we investigated if the isoform 2 of the Na+/H+ exchanger (NHE2), the main ion transporter involved in RVI responses, contributed to the AQP2-increased renal cell proliferation. Two cortical collecting duct cell lines were used: WT-RCCD1 (not expressing AQPs) and AQP2-RCCD1 (transfected with AQP2). We here demonstrate, for the first time, that AQP2-expressing cells present both higher intracellular pH and higher NHE2 protein expression than WT-RCCD1 cells. In AQP2-expresing cells NHE2 inhibition decreased cell proliferation and delayed cell cycle progression by slowing S and G2/M phases. We also observed that only in AQP2-expressing cells a NHE2-dependent RVI response was activated in the S phase. These observations suggest that the AQP2-increased proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2. Therefore, we propose that the accelerated proliferation of AQP2-expressing cells requires a coordinated modulation of the RVD/RVI activity that contributes to cell volume changes during cell cycle progression.Fil: Rivarola, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Di Giusto, Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Christensen, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Ford, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Capurro, Claudia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaWiley-liss, Div John Wiley & Sons Inc2016-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47443Rivarola, Valeria; Di Giusto, Gisela; Christensen, María José; Ford, Paula; Capurro, Claudia Graciela; AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 5; 5-2016; 967-9780730-2312CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/jcb.25602info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25602info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:07:39Zoai:ri.conicet.gov.ar:11336/47443instacron: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:34982025-09-03 10:07:40.024CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
title AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
spellingShingle AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
Rivarola, Valeria
Aqp2
Cell Proliferation
Nhe2
Regulatory Volume Increase
title_short AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
title_full AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
title_fullStr AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
title_full_unstemmed AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
title_sort AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2
dc.creator.none.fl_str_mv Rivarola, Valeria
Di Giusto, Gisela
Christensen, María José
Ford, Paula
Capurro, Claudia Graciela
author Rivarola, Valeria
author_facet Rivarola, Valeria
Di Giusto, Gisela
Christensen, María José
Ford, Paula
Capurro, Claudia Graciela
author_role author
author2 Di Giusto, Gisela
Christensen, María José
Ford, Paula
Capurro, Claudia Graciela
author2_role author
author
author
author
dc.subject.none.fl_str_mv Aqp2
Cell Proliferation
Nhe2
Regulatory Volume Increase
topic Aqp2
Cell Proliferation
Nhe2
Regulatory Volume Increase
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv We have previously shown in renal cells that expression of the water channel Aquaporin 2 (AQP2) increases the rate of cell proliferation by shortening the transit time through the S and G2/M phases of the cell cycle. This acceleration is due, at least in part; to a down-regulation of regulatory volume decrease (RVD) mechanisms when volume needs to be increased in order to proceed into the S phase. We hypothesize that in order to augment cell volume, RVD mechanisms may be overtaken by regulatory volume increase mechanisms (RVI). In this study, we investigated if the isoform 2 of the Na+/H+ exchanger (NHE2), the main ion transporter involved in RVI responses, contributed to the AQP2-increased renal cell proliferation. Two cortical collecting duct cell lines were used: WT-RCCD1 (not expressing AQPs) and AQP2-RCCD1 (transfected with AQP2). We here demonstrate, for the first time, that AQP2-expressing cells present both higher intracellular pH and higher NHE2 protein expression than WT-RCCD1 cells. In AQP2-expresing cells NHE2 inhibition decreased cell proliferation and delayed cell cycle progression by slowing S and G2/M phases. We also observed that only in AQP2-expressing cells a NHE2-dependent RVI response was activated in the S phase. These observations suggest that the AQP2-increased proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2. Therefore, we propose that the accelerated proliferation of AQP2-expressing cells requires a coordinated modulation of the RVD/RVI activity that contributes to cell volume changes during cell cycle progression.
Fil: Rivarola, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Di Giusto, Gisela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Christensen, María José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Ford, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Capurro, Claudia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
description We have previously shown in renal cells that expression of the water channel Aquaporin 2 (AQP2) increases the rate of cell proliferation by shortening the transit time through the S and G2/M phases of the cell cycle. This acceleration is due, at least in part; to a down-regulation of regulatory volume decrease (RVD) mechanisms when volume needs to be increased in order to proceed into the S phase. We hypothesize that in order to augment cell volume, RVD mechanisms may be overtaken by regulatory volume increase mechanisms (RVI). In this study, we investigated if the isoform 2 of the Na+/H+ exchanger (NHE2), the main ion transporter involved in RVI responses, contributed to the AQP2-increased renal cell proliferation. Two cortical collecting duct cell lines were used: WT-RCCD1 (not expressing AQPs) and AQP2-RCCD1 (transfected with AQP2). We here demonstrate, for the first time, that AQP2-expressing cells present both higher intracellular pH and higher NHE2 protein expression than WT-RCCD1 cells. In AQP2-expresing cells NHE2 inhibition decreased cell proliferation and delayed cell cycle progression by slowing S and G2/M phases. We also observed that only in AQP2-expressing cells a NHE2-dependent RVI response was activated in the S phase. These observations suggest that the AQP2-increased proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2. Therefore, we propose that the accelerated proliferation of AQP2-expressing cells requires a coordinated modulation of the RVD/RVI activity that contributes to cell volume changes during cell cycle progression.
publishDate 2016
dc.date.none.fl_str_mv 2016-05
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/11336/47443
Rivarola, Valeria; Di Giusto, Gisela; Christensen, María José; Ford, Paula; Capurro, Claudia Graciela; AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 5; 5-2016; 967-978
0730-2312
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47443
identifier_str_mv Rivarola, Valeria; Di Giusto, Gisela; Christensen, María José; Ford, Paula; Capurro, Claudia Graciela; AQP2-induced acceleration of renal cell proliferation involves the activation of a regulatory volume increase mechanism dependent on NHE2; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 118; 5; 5-2016; 967-978
0730-2312
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1002/jcb.25602
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.25602
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
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
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 13.13397

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