The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus

Autores
Freitag, Nancy; Tirado González, Irene; Barrientos, Gabriela Laura; Cohen, Marie; Daher, Silvia; Goldman Wohl, Debra; Mincheva Nilsson, Lucia; John, Constance M.; Jeschke, Udo; Blois, Sandra M.
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Problem: From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study: In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g, HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results: Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion: Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.
Fil: Freitag, Nancy. Charité - Universitätsmedizin; Alemania
Fil: Tirado González, Irene. Charité - Universitätsmedizin; Alemania
Fil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Cohen, Marie. Hôpitaux Universitaires de Genève; Suiza
Fil: Daher, Silvia. Universidade Federal de Sao Paulo; Brasil
Fil: Goldman Wohl, Debra. Hadassah-Hebrew University Medical Center; Israel
Fil: Mincheva Nilsson, Lucia. Universidad de Umea; Suecia
Fil: John, Constance M.. MandalMed, Inc; Estados Unidos
Fil: Jeschke, Udo. Klinikum Der Universität München; Alemania
Fil: Blois, Sandra M.. Charité – Universitätsmedizin Berlin; Alemania. University Medical Center Hamburg-Eppendorf; Alemania
Materia
GAL-3
PATHOLOGICAL PREGNANCY
PLACENTA
TROPHOBLAST
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/169979
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitusFreitag, NancyTirado González, IreneBarrientos, Gabriela LauraCohen, MarieDaher, SilviaGoldman Wohl, DebraMincheva Nilsson, LuciaJohn, Constance M.Jeschke, UdoBlois, Sandra M.GAL-3PATHOLOGICAL PREGNANCYPLACENTATROPHOBLASThttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Problem: From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study: In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g, HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results: Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion: Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.Fil: Freitag, Nancy. Charité - Universitätsmedizin; AlemaniaFil: Tirado González, Irene. Charité - Universitätsmedizin; AlemaniaFil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; ArgentinaFil: Cohen, Marie. Hôpitaux Universitaires de Genève; SuizaFil: Daher, Silvia. Universidade Federal de Sao Paulo; BrasilFil: Goldman Wohl, Debra. Hadassah-Hebrew University Medical Center; IsraelFil: Mincheva Nilsson, Lucia. Universidad de Umea; SueciaFil: John, Constance M.. MandalMed, Inc; Estados UnidosFil: Jeschke, Udo. Klinikum Der Universität München; AlemaniaFil: Blois, Sandra M.. Charité – Universitätsmedizin Berlin; Alemania. University Medical Center Hamburg-Eppendorf; AlemaniaWiley Blackwell Publishing, Inc2020-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/169979Freitag, Nancy; Tirado González, Irene; Barrientos, Gabriela Laura; Cohen, Marie; Daher, Silvia; et al.; The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus; Wiley Blackwell Publishing, Inc; American Journal of Reproductive Immunology; 84; 6; 12-2020; 1-91046-7408CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1111/aji.13311info:eu-repo/semantics/altIdentifier/doi/10.1111/aji.13311info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:55:21Zoai:ri.conicet.gov.ar:11336/169979instacron: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 09:55:21.627CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
title The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
spellingShingle The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
Freitag, Nancy
GAL-3
PATHOLOGICAL PREGNANCY
PLACENTA
TROPHOBLAST
title_short The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
title_full The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
title_fullStr The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
title_full_unstemmed The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
title_sort The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus
dc.creator.none.fl_str_mv Freitag, Nancy
Tirado González, Irene
Barrientos, Gabriela Laura
Cohen, Marie
Daher, Silvia
Goldman Wohl, Debra
Mincheva Nilsson, Lucia
John, Constance M.
Jeschke, Udo
Blois, Sandra M.
author Freitag, Nancy
author_facet Freitag, Nancy
Tirado González, Irene
Barrientos, Gabriela Laura
Cohen, Marie
Daher, Silvia
Goldman Wohl, Debra
Mincheva Nilsson, Lucia
John, Constance M.
Jeschke, Udo
Blois, Sandra M.
author_role author
author2 Tirado González, Irene
Barrientos, Gabriela Laura
Cohen, Marie
Daher, Silvia
Goldman Wohl, Debra
Mincheva Nilsson, Lucia
John, Constance M.
Jeschke, Udo
Blois, Sandra M.
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv GAL-3
PATHOLOGICAL PREGNANCY
PLACENTA
TROPHOBLAST
topic GAL-3
PATHOLOGICAL PREGNANCY
PLACENTA
TROPHOBLAST
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Problem: From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study: In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g, HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results: Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion: Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.
Fil: Freitag, Nancy. Charité - Universitätsmedizin; Alemania
Fil: Tirado González, Irene. Charité - Universitätsmedizin; Alemania
Fil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Cohen, Marie. Hôpitaux Universitaires de Genève; Suiza
Fil: Daher, Silvia. Universidade Federal de Sao Paulo; Brasil
Fil: Goldman Wohl, Debra. Hadassah-Hebrew University Medical Center; Israel
Fil: Mincheva Nilsson, Lucia. Universidad de Umea; Suecia
Fil: John, Constance M.. MandalMed, Inc; Estados Unidos
Fil: Jeschke, Udo. Klinikum Der Universität München; Alemania
Fil: Blois, Sandra M.. Charité – Universitätsmedizin Berlin; Alemania. University Medical Center Hamburg-Eppendorf; Alemania
description Problem: From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation. Method of study: In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g, HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM). Results: Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM. Conclusion: Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome.
publishDate 2020
dc.date.none.fl_str_mv 2020-12
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/11336/169979
Freitag, Nancy; Tirado González, Irene; Barrientos, Gabriela Laura; Cohen, Marie; Daher, Silvia; et al.; The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus; Wiley Blackwell Publishing, Inc; American Journal of Reproductive Immunology; 84; 6; 12-2020; 1-9
1046-7408
CONICET Digital
CONICET
url http://hdl.handle.net/11336/169979
identifier_str_mv Freitag, Nancy; Tirado González, Irene; Barrientos, Gabriela Laura; Cohen, Marie; Daher, Silvia; et al.; The chimera-type galectin-3 is a positive modulator of trophoblast functions with dysregulated expression in gestational diabetes mellitus; Wiley Blackwell Publishing, Inc; American Journal of Reproductive Immunology; 84; 6; 12-2020; 1-9
1046-7408
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://onlinelibrary.wiley.com/doi/10.1111/aji.13311
info:eu-repo/semantics/altIdentifier/doi/10.1111/aji.13311
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
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_ 1842269340311748608
score 13.13397

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