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
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/289250
Ver los metadatos del registro completo
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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. |
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2025 |
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2025-01 |
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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 |
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http://hdl.handle.net/11336/289250 |
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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 |
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