CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas

Autores
Castro-Parodi, Mauricio Omar; Levi, Lorena Natalia; Dietrich, Valeria; Zotta, Elsa; Damiano, Alicia Ermelinda
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Preeclampsia (PE) is a hypertensive disorder unique to human pregnancy. Although its causes remain unclear, it is known that altered placental villous angiogenesis and a poorly developed fetoplacental vasculature can affect the transport functions of the syncytiotrophoblast (hST). We have previously observed that in preeclamptic placentas there is an increase in AQP9 protein expression, with a lack of functionality. Up to now, the mechanisms for AQP9 regulation and the role of AQP9 in the human placenta remain unknown. However, there is strong evidence that the cystic fibrosis transmembrane conductance regulator (CFTR) regulates AQP9 functionality. Objective: Here, we studied CFTR expression and localization in hST from preeclamptic placentas in order to investigate if alterations in CFTR may be associated with the lack of activity of AQP9 observed in PE. Methods: The expression of CFTR in normal and preeclamptic placentas was determined by Western Blot and immunohistochemistry, and CFTR-AQP9 co-localization was determined by immunoflurescence. Water uptake experiments were performed using explants from human normal term and preeclamptic placentas treated with CFTR inhibitors. Results: We found that CFTR expression significantly decreased in preeclamptic placentas, and that the hST apical labeling almost disappeared, losing its co-localization with AQP9. Functional experiments demonstrated that water uptake diminished in normal term explants incubated with CFTR inhibitors. Conclusions: These results suggest that CFTR expression decreases in preeclampsia and may thus be implicated in the regulation of AQP9 activity.
Fil: Castro-Parodi, Mauricio Omar. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Levi, Lorena Natalia. 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: Dietrich, Valeria. 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: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Damiano, Alicia Ermelinda. 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
Materia
AQP9
CFTR
HUMAN PLACENTA
PREECLAMPSIA
SYNCYTIOTROPHOBLAST
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:11336/180239

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network_name_str CONICET Digital (CONICET)
spelling CFTR May Modulate AQP9 Functionality in Preeclamptic PlacentasCastro-Parodi, Mauricio OmarLevi, Lorena NataliaDietrich, ValeriaZotta, ElsaDamiano, Alicia ErmelindaAQP9CFTRHUMAN PLACENTAPREECLAMPSIASYNCYTIOTROPHOBLASThttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Preeclampsia (PE) is a hypertensive disorder unique to human pregnancy. Although its causes remain unclear, it is known that altered placental villous angiogenesis and a poorly developed fetoplacental vasculature can affect the transport functions of the syncytiotrophoblast (hST). We have previously observed that in preeclamptic placentas there is an increase in AQP9 protein expression, with a lack of functionality. Up to now, the mechanisms for AQP9 regulation and the role of AQP9 in the human placenta remain unknown. However, there is strong evidence that the cystic fibrosis transmembrane conductance regulator (CFTR) regulates AQP9 functionality. Objective: Here, we studied CFTR expression and localization in hST from preeclamptic placentas in order to investigate if alterations in CFTR may be associated with the lack of activity of AQP9 observed in PE. Methods: The expression of CFTR in normal and preeclamptic placentas was determined by Western Blot and immunohistochemistry, and CFTR-AQP9 co-localization was determined by immunoflurescence. Water uptake experiments were performed using explants from human normal term and preeclamptic placentas treated with CFTR inhibitors. Results: We found that CFTR expression significantly decreased in preeclamptic placentas, and that the hST apical labeling almost disappeared, losing its co-localization with AQP9. Functional experiments demonstrated that water uptake diminished in normal term explants incubated with CFTR inhibitors. Conclusions: These results suggest that CFTR expression decreases in preeclampsia and may thus be implicated in the regulation of AQP9 activity.Fil: Castro-Parodi, Mauricio Omar. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Levi, Lorena Natalia. 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: Dietrich, Valeria. 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: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Damiano, Alicia Ermelinda. 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; ArgentinaElsevier2009-07info: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/11336/180239Castro-Parodi, Mauricio Omar; Levi, Lorena Natalia; Dietrich, Valeria; Zotta, Elsa; Damiano, Alicia Ermelinda; CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas; Elsevier; Placenta; 30; 7; 7-2009; 642-6480143-4004CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.placenta.2009.04.012info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:49:11Zoai:ri.conicet.gov.ar:11336/180239instacron: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 09:49:12.298CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
title CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
spellingShingle CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
Castro-Parodi, Mauricio Omar
AQP9
CFTR
HUMAN PLACENTA
PREECLAMPSIA
SYNCYTIOTROPHOBLAST
title_short CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
title_full CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
title_fullStr CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
title_full_unstemmed CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
title_sort CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas
dc.creator.none.fl_str_mv Castro-Parodi, Mauricio Omar
Levi, Lorena Natalia
Dietrich, Valeria
Zotta, Elsa
Damiano, Alicia Ermelinda
author Castro-Parodi, Mauricio Omar
author_facet Castro-Parodi, Mauricio Omar
Levi, Lorena Natalia
Dietrich, Valeria
Zotta, Elsa
Damiano, Alicia Ermelinda
author_role author
author2 Levi, Lorena Natalia
Dietrich, Valeria
Zotta, Elsa
Damiano, Alicia Ermelinda
author2_role author
author
author
author
dc.subject.none.fl_str_mv AQP9
CFTR
HUMAN PLACENTA
PREECLAMPSIA
SYNCYTIOTROPHOBLAST
topic AQP9
CFTR
HUMAN PLACENTA
PREECLAMPSIA
SYNCYTIOTROPHOBLAST
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Preeclampsia (PE) is a hypertensive disorder unique to human pregnancy. Although its causes remain unclear, it is known that altered placental villous angiogenesis and a poorly developed fetoplacental vasculature can affect the transport functions of the syncytiotrophoblast (hST). We have previously observed that in preeclamptic placentas there is an increase in AQP9 protein expression, with a lack of functionality. Up to now, the mechanisms for AQP9 regulation and the role of AQP9 in the human placenta remain unknown. However, there is strong evidence that the cystic fibrosis transmembrane conductance regulator (CFTR) regulates AQP9 functionality. Objective: Here, we studied CFTR expression and localization in hST from preeclamptic placentas in order to investigate if alterations in CFTR may be associated with the lack of activity of AQP9 observed in PE. Methods: The expression of CFTR in normal and preeclamptic placentas was determined by Western Blot and immunohistochemistry, and CFTR-AQP9 co-localization was determined by immunoflurescence. Water uptake experiments were performed using explants from human normal term and preeclamptic placentas treated with CFTR inhibitors. Results: We found that CFTR expression significantly decreased in preeclamptic placentas, and that the hST apical labeling almost disappeared, losing its co-localization with AQP9. Functional experiments demonstrated that water uptake diminished in normal term explants incubated with CFTR inhibitors. Conclusions: These results suggest that CFTR expression decreases in preeclampsia and may thus be implicated in the regulation of AQP9 activity.
Fil: Castro-Parodi, Mauricio Omar. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Levi, Lorena Natalia. 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: Dietrich, Valeria. 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: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Damiano, Alicia Ermelinda. 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
description Preeclampsia (PE) is a hypertensive disorder unique to human pregnancy. Although its causes remain unclear, it is known that altered placental villous angiogenesis and a poorly developed fetoplacental vasculature can affect the transport functions of the syncytiotrophoblast (hST). We have previously observed that in preeclamptic placentas there is an increase in AQP9 protein expression, with a lack of functionality. Up to now, the mechanisms for AQP9 regulation and the role of AQP9 in the human placenta remain unknown. However, there is strong evidence that the cystic fibrosis transmembrane conductance regulator (CFTR) regulates AQP9 functionality. Objective: Here, we studied CFTR expression and localization in hST from preeclamptic placentas in order to investigate if alterations in CFTR may be associated with the lack of activity of AQP9 observed in PE. Methods: The expression of CFTR in normal and preeclamptic placentas was determined by Western Blot and immunohistochemistry, and CFTR-AQP9 co-localization was determined by immunoflurescence. Water uptake experiments were performed using explants from human normal term and preeclamptic placentas treated with CFTR inhibitors. Results: We found that CFTR expression significantly decreased in preeclamptic placentas, and that the hST apical labeling almost disappeared, losing its co-localization with AQP9. Functional experiments demonstrated that water uptake diminished in normal term explants incubated with CFTR inhibitors. Conclusions: These results suggest that CFTR expression decreases in preeclampsia and may thus be implicated in the regulation of AQP9 activity.
publishDate 2009
dc.date.none.fl_str_mv 2009-07
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/11336/180239
Castro-Parodi, Mauricio Omar; Levi, Lorena Natalia; Dietrich, Valeria; Zotta, Elsa; Damiano, Alicia Ermelinda; CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas; Elsevier; Placenta; 30; 7; 7-2009; 642-648
0143-4004
CONICET Digital
CONICET
url http://hdl.handle.net/11336/180239
identifier_str_mv Castro-Parodi, Mauricio Omar; Levi, Lorena Natalia; Dietrich, Valeria; Zotta, Elsa; Damiano, Alicia Ermelinda; CFTR May Modulate AQP9 Functionality in Preeclamptic Placentas; Elsevier; Placenta; 30; 7; 7-2009; 642-648
0143-4004
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.placenta.2009.04.012
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 Elsevier
publisher.none.fl_str_mv Elsevier
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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