Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model

Autores
Prados, Maria Belen; Solano, Maria Emilia; Friebe, A.; Blois, Sandra M.; Arck, Petra Clara; Miranda, Silvia Esther
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1+ vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.
Fil: Prados, Maria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Solano, Maria Emilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universitat Hamburg; Alemania
Fil: Friebe, A.. Ruhr Universität Bochum; Alemania. Universität zu Berlin; Alemania
Fil: Blois, Sandra M.. Universität zu Berlin; Alemania
Fil: Arck, Petra Clara. Universitat Hamburg; Alemania
Fil: Miranda, Silvia Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
Materia
Adhesion Molecules
Inflammation
Pecam
Pregnancy
Vessels
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/67576
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse modelPrados, Maria BelenSolano, Maria EmiliaFriebe, A.Blois, Sandra M.Arck, Petra ClaraMiranda, Silvia EstherAdhesion MoleculesInflammationPecamPregnancyVesselshttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1+ vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.Fil: Prados, Maria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Solano, Maria Emilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universitat Hamburg; AlemaniaFil: Friebe, A.. Ruhr Universität Bochum; Alemania. Universität zu Berlin; AlemaniaFil: Blois, Sandra M.. Universität zu Berlin; AlemaniaFil: Arck, Petra Clara. Universitat Hamburg; AlemaniaFil: Miranda, Silvia Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaElsevier Ireland2011-05info: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/11336/67576Prados, Maria Belen; Solano, Maria Emilia; Friebe, A.; Blois, Sandra M.; Arck, Petra Clara; et al.; Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model; Elsevier Ireland; Journal of Reproductive Immunology; 89; 2; 5-2011; 207-2110165-0378CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.jri.2011.01.021info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0165037811000532info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-02-06T12:32:12Zoai:ri.conicet.gov.ar:11336/67576instacron: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:34982026-02-06 12:32:13.026CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
title Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
spellingShingle Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
Prados, Maria Belen
Adhesion Molecules
Inflammation
Pecam
Pregnancy
Vessels
title_short Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
title_full Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
title_fullStr Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
title_full_unstemmed Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
title_sort Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model
dc.creator.none.fl_str_mv Prados, Maria Belen
Solano, Maria Emilia
Friebe, A.
Blois, Sandra M.
Arck, Petra Clara
Miranda, Silvia Esther
author Prados, Maria Belen
author_facet Prados, Maria Belen
Solano, Maria Emilia
Friebe, A.
Blois, Sandra M.
Arck, Petra Clara
Miranda, Silvia Esther
author_role author
author2 Solano, Maria Emilia
Friebe, A.
Blois, Sandra M.
Arck, Petra Clara
Miranda, Silvia Esther
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Adhesion Molecules
Inflammation
Pecam
Pregnancy
Vessels
topic Adhesion Molecules
Inflammation
Pecam
Pregnancy
Vessels
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1+ vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.
Fil: Prados, Maria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Solano, Maria Emilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universitat Hamburg; Alemania
Fil: Friebe, A.. Ruhr Universität Bochum; Alemania. Universität zu Berlin; Alemania
Fil: Blois, Sandra M.. Universität zu Berlin; Alemania
Fil: Arck, Petra Clara. Universitat Hamburg; Alemania
Fil: Miranda, Silvia Esther. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
description Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1+ vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.
publishDate 2011
dc.date.none.fl_str_mv 2011-05
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/11336/67576
Prados, Maria Belen; Solano, Maria Emilia; Friebe, A.; Blois, Sandra M.; Arck, Petra Clara; et al.; Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model; Elsevier Ireland; Journal of Reproductive Immunology; 89; 2; 5-2011; 207-211
0165-0378
CONICET Digital
CONICET
url http://hdl.handle.net/11336/67576
identifier_str_mv Prados, Maria Belen; Solano, Maria Emilia; Friebe, A.; Blois, Sandra M.; Arck, Petra Clara; et al.; Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model; Elsevier Ireland; Journal of Reproductive Immunology; 89; 2; 5-2011; 207-211
0165-0378
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.jri.2011.01.021
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0165037811000532
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
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_ 1856403167293472768
score 13.106097

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