The role of aqp3 in amnion cells exposed to an osmotic stress

Autores
Di Paola, Mauricio Adriel; Sierra, M. N.; Fernandez, N.; Erlejman, A.; Castro Parodi, M.; Damiano, Alicia Ermelinda
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
INTRODUCTION: AQPs in fetal membranes have been proposed to regulate the amniotic fluid volume. Altered expression of these proteins might be associated with oligo and polyhydramnios syndromes. However, we recently observed that the blocking of AQP3 did not prevent cell swelling in amnion cells. In addition, under osmotic stress the pattern expression of amnion AQP3 was different from other AQPs, suggesting a different role for this protein. OBJETIVE: To study the regulation of AQP3 and its role in the amnion.METHODS: Amnion-derived WISH cells were cultured in hypo (150 mOsm) and hyperosmolar (400 mOsm) conditions. Levels of phosphorylated ERK (pERK), JUNK (pJNK) and p38 (p-p38) were studied. Nf-ĸB and tonEBP expressions were assessed in nuclear and cytosolic fractions. AQP3 expression was analyzed after the inhibition of Nf-ĸB and tonEBP pathways with Sodium Salicylate and Cyclosporine-A, respectively. Cell viability was studied by MTT assay. Apoptosis was studied by TUNEL assay and Bax/Bcl-2 ratio after the inhibition of AQP3 using CuSO4 or the specific siRNA. RESULTS: pERK levels increased in hyperosmolarity and did not change in hypoosmolarity (p<0.001; n=6). No significant differences were observed in p-p38 and pJNK (ns; n=6). Nf-ĸB and tonEBP expressions increased in nuclear fraction only in hyperosmolarity (p<0.05; n=5; p<0.01; n=5). In this condition, the blocking of Nf-ĸB pathway increased AQP3 expression (p<0.001; n=5) compared to controls, while the inhibition of tonEBP pathway did not modify its expression. Regarding cell viability in hiperosmolarity, the blocking of AQP3 decreased MTT incorporation (p<0.01; n=8). Moreover, Bax/Bcl-2 ratio and the number of apoptotic nuclei increased after CuSO4 treatment (p<0.001; n=5; p<0.001; n=9) and AQP3 silencing (p<0.05; n=5; p<0.01; n=10).CONCLUSION: Our findings suggest that AQP3 may have an important role in the survival of the amniotic cells and its expression may be regulated by ERK, Nf-ĸB and tonEBP pathways.
Fil: Di Paola, Mauricio Adriel. 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, M. N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Fernandez, N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Erlejman, A.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Castro Parodi, M.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; 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
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Asociación Argentina de Fisiología
Materia
AQUAPORIN 3
HUMAN AMNION
PLACENTA
OSMOTIC STRESS
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:11336/195037
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/195037
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The role of aqp3 in amnion cells exposed to an osmotic stressDi Paola, Mauricio AdrielSierra, M. N.Fernandez, N.Erlejman, A.Castro Parodi, M.Damiano, Alicia ErmelindaAQUAPORIN 3HUMAN AMNIONPLACENTAOSMOTIC STRESShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1INTRODUCTION: AQPs in fetal membranes have been proposed to regulate the amniotic fluid volume. Altered expression of these proteins might be associated with oligo and polyhydramnios syndromes. However, we recently observed that the blocking of AQP3 did not prevent cell swelling in amnion cells. In addition, under osmotic stress the pattern expression of amnion AQP3 was different from other AQPs, suggesting a different role for this protein. OBJETIVE: To study the regulation of AQP3 and its role in the amnion.METHODS: Amnion-derived WISH cells were cultured in hypo (150 mOsm) and hyperosmolar (400 mOsm) conditions. Levels of phosphorylated ERK (pERK), JUNK (pJNK) and p38 (p-p38) were studied. Nf-ĸB and tonEBP expressions were assessed in nuclear and cytosolic fractions. AQP3 expression was analyzed after the inhibition of Nf-ĸB and tonEBP pathways with Sodium Salicylate and Cyclosporine-A, respectively. Cell viability was studied by MTT assay. Apoptosis was studied by TUNEL assay and Bax/Bcl-2 ratio after the inhibition of AQP3 using CuSO4 or the specific siRNA. RESULTS: pERK levels increased in hyperosmolarity and did not change in hypoosmolarity (p<0.001; n=6). No significant differences were observed in p-p38 and pJNK (ns; n=6). Nf-ĸB and tonEBP expressions increased in nuclear fraction only in hyperosmolarity (p<0.05; n=5; p<0.01; n=5). In this condition, the blocking of Nf-ĸB pathway increased AQP3 expression (p<0.001; n=5) compared to controls, while the inhibition of tonEBP pathway did not modify its expression. Regarding cell viability in hiperosmolarity, the blocking of AQP3 decreased MTT incorporation (p<0.01; n=8). Moreover, Bax/Bcl-2 ratio and the number of apoptotic nuclei increased after CuSO4 treatment (p<0.001; n=5; p<0.001; n=9) and AQP3 silencing (p<0.05; n=5; p<0.01; n=10).CONCLUSION: Our findings suggest that AQP3 may have an important role in the survival of the amniotic cells and its expression may be regulated by ERK, Nf-ĸB and tonEBP pathways.Fil: Di Paola, Mauricio Adriel. 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, M. N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Fernandez, N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Erlejman, A.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Castro Parodi, M.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; 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 FisiologíaBuenos AiresArgentinaSociedad 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/pdfapplication/pdfhttp://hdl.handle.net/11336/195037The role of aqp3 in amnion cells exposed to an osmotic stress; 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; Buenos Aires; Argentina; 2020; 207-207CONICET DigitalCONICETengNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:56:45Zoai:ri.conicet.gov.ar:11336/195037instacron: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:34982025-10-22 11:56:45.459CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The role of aqp3 in amnion cells exposed to an osmotic stress
title The role of aqp3 in amnion cells exposed to an osmotic stress
spellingShingle The role of aqp3 in amnion cells exposed to an osmotic stress
Di Paola, Mauricio Adriel
AQUAPORIN 3
HUMAN AMNION
PLACENTA
OSMOTIC STRESS
title_short The role of aqp3 in amnion cells exposed to an osmotic stress
title_full The role of aqp3 in amnion cells exposed to an osmotic stress
title_fullStr The role of aqp3 in amnion cells exposed to an osmotic stress
title_full_unstemmed The role of aqp3 in amnion cells exposed to an osmotic stress
title_sort The role of aqp3 in amnion cells exposed to an osmotic stress
dc.creator.none.fl_str_mv Di Paola, Mauricio Adriel
Sierra, M. N.
Fernandez, N.
Erlejman, A.
Castro Parodi, M.
Damiano, Alicia Ermelinda
author Di Paola, Mauricio Adriel
author_facet Di Paola, Mauricio Adriel
Sierra, M. N.
Fernandez, N.
Erlejman, A.
Castro Parodi, M.
Damiano, Alicia Ermelinda
author_role author
author2 Sierra, M. N.
Fernandez, N.
Erlejman, A.
Castro Parodi, M.
Damiano, Alicia Ermelinda
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv AQUAPORIN 3
HUMAN AMNION
PLACENTA
OSMOTIC STRESS
topic AQUAPORIN 3
HUMAN AMNION
PLACENTA
OSMOTIC STRESS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv INTRODUCTION: AQPs in fetal membranes have been proposed to regulate the amniotic fluid volume. Altered expression of these proteins might be associated with oligo and polyhydramnios syndromes. However, we recently observed that the blocking of AQP3 did not prevent cell swelling in amnion cells. In addition, under osmotic stress the pattern expression of amnion AQP3 was different from other AQPs, suggesting a different role for this protein. OBJETIVE: To study the regulation of AQP3 and its role in the amnion.METHODS: Amnion-derived WISH cells were cultured in hypo (150 mOsm) and hyperosmolar (400 mOsm) conditions. Levels of phosphorylated ERK (pERK), JUNK (pJNK) and p38 (p-p38) were studied. Nf-ĸB and tonEBP expressions were assessed in nuclear and cytosolic fractions. AQP3 expression was analyzed after the inhibition of Nf-ĸB and tonEBP pathways with Sodium Salicylate and Cyclosporine-A, respectively. Cell viability was studied by MTT assay. Apoptosis was studied by TUNEL assay and Bax/Bcl-2 ratio after the inhibition of AQP3 using CuSO4 or the specific siRNA. RESULTS: pERK levels increased in hyperosmolarity and did not change in hypoosmolarity (p<0.001; n=6). No significant differences were observed in p-p38 and pJNK (ns; n=6). Nf-ĸB and tonEBP expressions increased in nuclear fraction only in hyperosmolarity (p<0.05; n=5; p<0.01; n=5). In this condition, the blocking of Nf-ĸB pathway increased AQP3 expression (p<0.001; n=5) compared to controls, while the inhibition of tonEBP pathway did not modify its expression. Regarding cell viability in hiperosmolarity, the blocking of AQP3 decreased MTT incorporation (p<0.01; n=8). Moreover, Bax/Bcl-2 ratio and the number of apoptotic nuclei increased after CuSO4 treatment (p<0.001; n=5; p<0.001; n=9) and AQP3 silencing (p<0.05; n=5; p<0.01; n=10).CONCLUSION: Our findings suggest that AQP3 may have an important role in the survival of the amniotic cells and its expression may be regulated by ERK, Nf-ĸB and tonEBP pathways.
Fil: Di Paola, Mauricio Adriel. 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, M. N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Fil: Fernandez, N.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Erlejman, A.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Castro Parodi, M.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; 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
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Asociación Argentina de Fisiología
description INTRODUCTION: AQPs in fetal membranes have been proposed to regulate the amniotic fluid volume. Altered expression of these proteins might be associated with oligo and polyhydramnios syndromes. However, we recently observed that the blocking of AQP3 did not prevent cell swelling in amnion cells. In addition, under osmotic stress the pattern expression of amnion AQP3 was different from other AQPs, suggesting a different role for this protein. OBJETIVE: To study the regulation of AQP3 and its role in the amnion.METHODS: Amnion-derived WISH cells were cultured in hypo (150 mOsm) and hyperosmolar (400 mOsm) conditions. Levels of phosphorylated ERK (pERK), JUNK (pJNK) and p38 (p-p38) were studied. Nf-ĸB and tonEBP expressions were assessed in nuclear and cytosolic fractions. AQP3 expression was analyzed after the inhibition of Nf-ĸB and tonEBP pathways with Sodium Salicylate and Cyclosporine-A, respectively. Cell viability was studied by MTT assay. Apoptosis was studied by TUNEL assay and Bax/Bcl-2 ratio after the inhibition of AQP3 using CuSO4 or the specific siRNA. RESULTS: pERK levels increased in hyperosmolarity and did not change in hypoosmolarity (p<0.001; n=6). No significant differences were observed in p-p38 and pJNK (ns; n=6). Nf-ĸB and tonEBP expressions increased in nuclear fraction only in hyperosmolarity (p<0.05; n=5; p<0.01; n=5). In this condition, the blocking of Nf-ĸB pathway increased AQP3 expression (p<0.001; n=5) compared to controls, while the inhibition of tonEBP pathway did not modify its expression. Regarding cell viability in hiperosmolarity, the blocking of AQP3 decreased MTT incorporation (p<0.01; n=8). Moreover, Bax/Bcl-2 ratio and the number of apoptotic nuclei increased after CuSO4 treatment (p<0.001; n=5; p<0.001; n=9) and AQP3 silencing (p<0.05; n=5; p<0.01; n=10).CONCLUSION: Our findings suggest that AQP3 may have an important role in the survival of the amniotic cells and its expression may be regulated by ERK, Nf-ĸB and tonEBP pathways.
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
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/195037
The role of aqp3 in amnion cells exposed to an osmotic stress; 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; Buenos Aires; Argentina; 2020; 207-207
CONICET Digital
CONICET
url http://hdl.handle.net/11336/195037
identifier_str_mv The role of aqp3 in amnion cells exposed to an osmotic stress; 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; Buenos Aires; Argentina; 2020; 207-207
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
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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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