Aqp9 mediates lactate transport in human placenta as an alternative energy substrate
- Autores
- Medina Mora, Yollyseth Astrid; Sierra, Matias Nicolas; Anud, Carolina Valeria; Szpilbarg, Natalia; Damiano, Alicia Ermelinda
- Año de publicación
- 2020
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Emerging evidence shows that placental aquaporin-9 (AQP9) is notinvolved in the transfer of water between the mother and the fetus.However, its role in human placenta is still unknown. AQP9 is anaquaglyceroporin that also permeates other solutes such as lactate. Inbrain, AQP9 may transport lactate as an alternative energy substrate.OBJECTIVE: Our aim was to evaluate the participation of AQP9 inthe lactate transfer across the human placenta.METHODS: This study was approved by the ethics committee of theHospital Nacional Dr. Prof. A. Posadas. Explants from normal termplacentas were cultured in low glucose with or without L-lactate, andin presence and absence of AQP9 inhibitors (0.3 mM HgCl2, a general blocker of AQPs, or 0.5mM Phloretin, to block AQP9). Normalglucose medium was used as control. Cell viability was assessed byMTT assay and LDH release. Apoptosis indexes were analyzed byBax/Bcl-2 protein expression ratio and TUNEL assay.RESULTS: In low glucose medium, MTT decreased while LDHrelease did not change compared to controls, suggesting that celldeath is not due to necrosis. Moreover, Bax/Bcl-2 ratio and apoptoticnuclei increased (n=5, p <0.02) and the blocking of AQP9 did notabrogate apoptosis. However, when explants were cultured in lowglucose medium supplemented with L-lactate, explant viability andapoptotic indexes were similar to controls indicating that L-lactatecould be replacing glucose as an energy substrate. In this case, theblocking of AQP9 resulted in an increase in cell death (n=4, p <0.05),proposing that this protein has a role in lactate transport.CONCLUSION: Our results show that placental AQP9 may havea key role in lactate transport as an alternative energy substrate.Thus, the blocking of lactate transport mediated by AQP9 negativelyaffects the survival of trophoblast cells.
Fil: Medina Mora, Yollyseth Astrid. 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: Sierra, Matias Nicolas. 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. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Anud, Carolina Valeria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Szpilbarg, Natalia. 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: Damiano, Alicia Ermelinda. 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. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Asociación Argentina de Fisiología - Materia
-
AQP9
PLACENTA
LACTATE - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/199439
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Aqp9 mediates lactate transport in human placenta as an alternative energy substrateMedina Mora, Yollyseth AstridSierra, Matias NicolasAnud, Carolina ValeriaSzpilbarg, NataliaDamiano, Alicia ErmelindaAQP9PLACENTALACTATEhttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3Emerging evidence shows that placental aquaporin-9 (AQP9) is notinvolved in the transfer of water between the mother and the fetus.However, its role in human placenta is still unknown. AQP9 is anaquaglyceroporin that also permeates other solutes such as lactate. Inbrain, AQP9 may transport lactate as an alternative energy substrate.OBJECTIVE: Our aim was to evaluate the participation of AQP9 inthe lactate transfer across the human placenta.METHODS: This study was approved by the ethics committee of theHospital Nacional Dr. Prof. A. Posadas. Explants from normal termplacentas were cultured in low glucose with or without L-lactate, andin presence and absence of AQP9 inhibitors (0.3 mM HgCl2, a general blocker of AQPs, or 0.5mM Phloretin, to block AQP9). Normalglucose medium was used as control. Cell viability was assessed byMTT assay and LDH release. Apoptosis indexes were analyzed byBax/Bcl-2 protein expression ratio and TUNEL assay.RESULTS: In low glucose medium, MTT decreased while LDHrelease did not change compared to controls, suggesting that celldeath is not due to necrosis. Moreover, Bax/Bcl-2 ratio and apoptoticnuclei increased (n=5, p <0.02) and the blocking of AQP9 did notabrogate apoptosis. However, when explants were cultured in lowglucose medium supplemented with L-lactate, explant viability andapoptotic indexes were similar to controls indicating that L-lactatecould be replacing glucose as an energy substrate. In this case, theblocking of AQP9 resulted in an increase in cell death (n=4, p <0.05),proposing that this protein has a role in lactate transport.CONCLUSION: Our results show that placental AQP9 may havea key role in lactate transport as an alternative energy substrate.Thus, the blocking of lactate transport mediated by AQP9 negativelyaffects the survival of trophoblast cells.Fil: Medina Mora, Yollyseth Astrid. 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: Sierra, Matias Nicolas. 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. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Anud, Carolina Valeria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Szpilbarg, Natalia. 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: Damiano, Alicia Ermelinda. 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. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaLXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de FisiologíaArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaAsociación Argentina de FisiologíaFundación Revista Medicina2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/199439Aqp9 mediates lactate transport in human placenta as an alternative energy substrate; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 206-2060025-7680CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reunion-anualNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:47:56Zoai:ri.conicet.gov.ar:11336/199439instacron: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:34982025-09-29 10:47:56.579CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
title |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
spellingShingle |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate Medina Mora, Yollyseth Astrid AQP9 PLACENTA LACTATE |
title_short |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
title_full |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
title_fullStr |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
title_full_unstemmed |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
title_sort |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate |
dc.creator.none.fl_str_mv |
Medina Mora, Yollyseth Astrid Sierra, Matias Nicolas Anud, Carolina Valeria Szpilbarg, Natalia Damiano, Alicia Ermelinda |
author |
Medina Mora, Yollyseth Astrid |
author_facet |
Medina Mora, Yollyseth Astrid Sierra, Matias Nicolas Anud, Carolina Valeria Szpilbarg, Natalia Damiano, Alicia Ermelinda |
author_role |
author |
author2 |
Sierra, Matias Nicolas Anud, Carolina Valeria Szpilbarg, Natalia Damiano, Alicia Ermelinda |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
AQP9 PLACENTA LACTATE |
topic |
AQP9 PLACENTA LACTATE |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.5 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Emerging evidence shows that placental aquaporin-9 (AQP9) is notinvolved in the transfer of water between the mother and the fetus.However, its role in human placenta is still unknown. AQP9 is anaquaglyceroporin that also permeates other solutes such as lactate. Inbrain, AQP9 may transport lactate as an alternative energy substrate.OBJECTIVE: Our aim was to evaluate the participation of AQP9 inthe lactate transfer across the human placenta.METHODS: This study was approved by the ethics committee of theHospital Nacional Dr. Prof. A. Posadas. Explants from normal termplacentas were cultured in low glucose with or without L-lactate, andin presence and absence of AQP9 inhibitors (0.3 mM HgCl2, a general blocker of AQPs, or 0.5mM Phloretin, to block AQP9). Normalglucose medium was used as control. Cell viability was assessed byMTT assay and LDH release. Apoptosis indexes were analyzed byBax/Bcl-2 protein expression ratio and TUNEL assay.RESULTS: In low glucose medium, MTT decreased while LDHrelease did not change compared to controls, suggesting that celldeath is not due to necrosis. Moreover, Bax/Bcl-2 ratio and apoptoticnuclei increased (n=5, p <0.02) and the blocking of AQP9 did notabrogate apoptosis. However, when explants were cultured in lowglucose medium supplemented with L-lactate, explant viability andapoptotic indexes were similar to controls indicating that L-lactatecould be replacing glucose as an energy substrate. In this case, theblocking of AQP9 resulted in an increase in cell death (n=4, p <0.05),proposing that this protein has a role in lactate transport.CONCLUSION: Our results show that placental AQP9 may havea key role in lactate transport as an alternative energy substrate.Thus, the blocking of lactate transport mediated by AQP9 negativelyaffects the survival of trophoblast cells. Fil: Medina Mora, Yollyseth Astrid. 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: Sierra, Matias Nicolas. 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. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina Fil: Anud, Carolina Valeria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina Fil: Szpilbarg, Natalia. 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: Damiano, Alicia Ermelinda. 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. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología Argentina Sociedad Argentina de Investigación Clínica Sociedad Argentina de Inmunología Asociación Argentina de Fisiología |
description |
Emerging evidence shows that placental aquaporin-9 (AQP9) is notinvolved in the transfer of water between the mother and the fetus.However, its role in human placenta is still unknown. AQP9 is anaquaglyceroporin that also permeates other solutes such as lactate. Inbrain, AQP9 may transport lactate as an alternative energy substrate.OBJECTIVE: Our aim was to evaluate the participation of AQP9 inthe lactate transfer across the human placenta.METHODS: This study was approved by the ethics committee of theHospital Nacional Dr. Prof. A. Posadas. Explants from normal termplacentas were cultured in low glucose with or without L-lactate, andin presence and absence of AQP9 inhibitors (0.3 mM HgCl2, a general blocker of AQPs, or 0.5mM Phloretin, to block AQP9). Normalglucose medium was used as control. Cell viability was assessed byMTT assay and LDH release. Apoptosis indexes were analyzed byBax/Bcl-2 protein expression ratio and TUNEL assay.RESULTS: In low glucose medium, MTT decreased while LDHrelease did not change compared to controls, suggesting that celldeath is not due to necrosis. Moreover, Bax/Bcl-2 ratio and apoptoticnuclei increased (n=5, p <0.02) and the blocking of AQP9 did notabrogate apoptosis. However, when explants were cultured in lowglucose medium supplemented with L-lactate, explant viability andapoptotic indexes were similar to controls indicating that L-lactatecould be replacing glucose as an energy substrate. In this case, theblocking of AQP9 resulted in an increase in cell death (n=4, p <0.05),proposing that this protein has a role in lactate transport.CONCLUSION: Our results show that placental AQP9 may havea key role in lactate transport as an alternative energy substrate.Thus, the blocking of lactate transport mediated by AQP9 negativelyaffects the survival of trophoblast cells. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/conferenceObject Reunión Journal http://purl.org/coar/resource_type/c_5794 info:ar-repo/semantics/documentoDeConferencia |
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publishedVersion |
format |
conferenceObject |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/199439 Aqp9 mediates lactate transport in human placenta as an alternative energy substrate; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 206-206 0025-7680 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/199439 |
identifier_str_mv |
Aqp9 mediates lactate transport in human placenta as an alternative energy substrate; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 206-206 0025-7680 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
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info:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reunion-anual |
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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Nacional |
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Fundación Revista Medicina |
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Fundación Revista Medicina |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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