Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model

Autores
Oronel, Lucas Humberto; Ortiz, Maria; Yarza, Carolina Andrea; Gayone, Sofía; Davio, Carlos Alberto; Majowicz, Mónica Patricia; Albertoni Borghese, Maria Florencia
Año de publicación
2025
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silentin the early stages and gradually progresses, inducing renal physiological and structuralalterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ inunderlying etiology, time of onset, and associated diseases. The 0.25% adenine dietinduces progressive kidney damage, constituting an adequate model mimicking humanCKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate ifAQP2 expression is altered in an adenine-induced model of CKD in rats at early stages ofdevelopment (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2receptor antagonist) treatment. We showed an increased renal medullary AQP2 expressionat two weeks of adenine administration. This increase was mainly cytoplasmic, explainingthe increased urinary volume of CKD rats and suggesting a possible non-canonical role forAQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKDrats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightlyreduced BUN and plasma creatinine. On the other hand, the renal alterations induced byadenine in CKD rats were not prevented by Tolvaptan.
Fil: Oronel, Lucas Humberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Ortiz, Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Yarza, Carolina Andrea. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Gayone, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Majowicz, Mónica Patricia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Albertoni Borghese, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Materia
CHRONIC KIDNEY DISEASE
AQP2
TOLVAPTAN
V2 RECEPTOR
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:11336/289250

id CONICETDig_d439b973b7f1a06dc52f8fa1c3bd69ad
oai_identifier_str oai:ri.conicet.gov.ar:11336/289250
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease modelOronel, Lucas HumbertoOrtiz, MariaYarza, Carolina AndreaGayone, SofíaDavio, Carlos AlbertoMajowicz, Mónica PatriciaAlbertoni Borghese, Maria FlorenciaCHRONIC KIDNEY DISEASEAQP2TOLVAPTANV2 RECEPTORhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silentin the early stages and gradually progresses, inducing renal physiological and structuralalterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ inunderlying etiology, time of onset, and associated diseases. The 0.25% adenine dietinduces progressive kidney damage, constituting an adequate model mimicking humanCKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate ifAQP2 expression is altered in an adenine-induced model of CKD in rats at early stages ofdevelopment (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2receptor antagonist) treatment. We showed an increased renal medullary AQP2 expressionat two weeks of adenine administration. This increase was mainly cytoplasmic, explainingthe increased urinary volume of CKD rats and suggesting a possible non-canonical role forAQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKDrats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightlyreduced BUN and plasma creatinine. On the other hand, the renal alterations induced byadenine in CKD rats were not prevented by Tolvaptan.Fil: Oronel, Lucas Humberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Ortiz, Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Yarza, Carolina Andrea. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Gayone, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Majowicz, Mónica Patricia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Albertoni Borghese, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaPublic Library of Science2025-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/289250Oronel, Lucas Humberto; Ortiz, Maria; Yarza, Carolina Andrea; Gayone, Sofía; Davio, Carlos Alberto; et al.; Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model; Public Library of Science; Plos One; 20; 1; 1-2025; 1-171932-6203CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://dx.plos.org/10.1371/journal.pone.0314827info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0314827info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-06-17T09:41:56Zoai:ri.conicet.gov.ar:11336/289250instacron: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:34982026-06-17 09:41:56.378CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
title Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
spellingShingle Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
Oronel, Lucas Humberto
CHRONIC KIDNEY DISEASE
AQP2
TOLVAPTAN
V2 RECEPTOR
title_short Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
title_full Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
title_fullStr Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
title_full_unstemmed Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
title_sort Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model
dc.creator.none.fl_str_mv Oronel, Lucas Humberto
Ortiz, Maria
Yarza, Carolina Andrea
Gayone, Sofía
Davio, Carlos Alberto
Majowicz, Mónica Patricia
Albertoni Borghese, Maria Florencia
author Oronel, Lucas Humberto
author_facet Oronel, Lucas Humberto
Ortiz, Maria
Yarza, Carolina Andrea
Gayone, Sofía
Davio, Carlos Alberto
Majowicz, Mónica Patricia
Albertoni Borghese, Maria Florencia
author_role author
author2 Ortiz, Maria
Yarza, Carolina Andrea
Gayone, Sofía
Davio, Carlos Alberto
Majowicz, Mónica Patricia
Albertoni Borghese, Maria Florencia
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv CHRONIC KIDNEY DISEASE
AQP2
TOLVAPTAN
V2 RECEPTOR
topic CHRONIC KIDNEY DISEASE
AQP2
TOLVAPTAN
V2 RECEPTOR
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silentin the early stages and gradually progresses, inducing renal physiological and structuralalterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ inunderlying etiology, time of onset, and associated diseases. The 0.25% adenine dietinduces progressive kidney damage, constituting an adequate model mimicking humanCKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate ifAQP2 expression is altered in an adenine-induced model of CKD in rats at early stages ofdevelopment (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2receptor antagonist) treatment. We showed an increased renal medullary AQP2 expressionat two weeks of adenine administration. This increase was mainly cytoplasmic, explainingthe increased urinary volume of CKD rats and suggesting a possible non-canonical role forAQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKDrats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightlyreduced BUN and plasma creatinine. On the other hand, the renal alterations induced byadenine in CKD rats were not prevented by Tolvaptan.
Fil: Oronel, Lucas Humberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Ortiz, Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Yarza, Carolina Andrea. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Gayone, Sofía. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Majowicz, Mónica Patricia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Albertoni Borghese, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
description Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silentin the early stages and gradually progresses, inducing renal physiological and structuralalterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ inunderlying etiology, time of onset, and associated diseases. The 0.25% adenine dietinduces progressive kidney damage, constituting an adequate model mimicking humanCKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate ifAQP2 expression is altered in an adenine-induced model of CKD in rats at early stages ofdevelopment (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2receptor antagonist) treatment. We showed an increased renal medullary AQP2 expressionat two weeks of adenine administration. This increase was mainly cytoplasmic, explainingthe increased urinary volume of CKD rats and suggesting a possible non-canonical role forAQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKDrats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightlyreduced BUN and plasma creatinine. On the other hand, the renal alterations induced byadenine in CKD rats were not prevented by Tolvaptan.
publishDate 2025
dc.date.none.fl_str_mv 2025-01
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/11336/289250
Oronel, Lucas Humberto; Ortiz, Maria; Yarza, Carolina Andrea; Gayone, Sofía; Davio, Carlos Alberto; et al.; Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model; Public Library of Science; Plos One; 20; 1; 1-2025; 1-17
1932-6203
CONICET Digital
CONICET
url http://hdl.handle.net/11336/289250
identifier_str_mv Oronel, Lucas Humberto; Ortiz, Maria; Yarza, Carolina Andrea; Gayone, Sofía; Davio, Carlos Alberto; et al.; Aquaporin-2 in the early stages of the adenine-induced chronic kidney disease model; Public Library of Science; Plos One; 20; 1; 1-2025; 1-17
1932-6203
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://dx.plos.org/10.1371/journal.pone.0314827
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0314827
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
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
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
_version_ 1868339045095964672
score 13.040872