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dc.contributor.author Beltrame, Jimena Soledad
dc.contributor.author Sordelli, Micaela Soledad
dc.contributor.author Cañumil, Vanesa Alejandra
dc.contributor.author Franchi, Ana Maria
dc.contributor.author Ribeiro, Maria Laura
dc.date.available 2018-11-27T19:13:07Z
dc.date.issued 2018-01
dc.identifier.citation Beltrame, Jimena Soledad; Sordelli, Micaela Soledad; Cañumil, Vanesa Alejandra; Franchi, Ana Maria; Ribeiro, Maria Laura; Lysophosphatidic acid-triggered pathways promote the acquisition of trophoblast endovascular phenotype in vitro; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Biochemistry; 119; 1; 1-2018; 758-772
dc.identifier.issn 0730-2312
dc.identifier.uri http://hdl.handle.net/11336/65372
dc.description.abstract Successful implantation and placentation requires that extravillous cytotrophoblast acquires an endovascular phenotype and remodels uterine spiral arteries. Defects in this mechanism correlate with severe obstetric complications as implantation failure and preeclampsia. Lysophosphatidic acid (LPA) participates in embryo implantation and contributes to vascular physiology in different biological systems. However, the role of LPA on trophoblast endovascular transformation has not been studied. Due to difficulties in studying human pregnancy in vivo, we adopted a pharmacological approach in vitro to investigate LPA action in various aspects of trophoblast endovascular response, such as the formation of endothelial capillary-like structures, migration, and proliferation. The HTR-8/SVneo cell line established from human first trimester cytotrophoblast was used to model the acquisition of the endovascular phenotype by the invading trophoblast. LPA increased HTR-8/SVneo tube formation, migration (wound healing assay and phalloidin staining) and proliferation (MTT assay). LPA G protein-coupled receptors, LPA1 and LPA3, were expressed in HTR-8/SVneo. By using selective antagonists, we showed that enhanced tubulogenesis was mediated by LPA3. In addition, cyclooxygenase-2 and inducible nitric oxide synthase pathways participated in LPA-stimulated tubulogenesis. Inducible nitric oxide synthase was activated downstream cyclooxygenase-2. Furthermore, prostaglandin E2 and a nitric oxide donor (SNAP) increased trophoblast tube formation in a concentration-dependent manner. Finally, we observed that cyclooxygenase-2 and inducible nitric oxide synthase were localized in the nucleus, and LPA did not modify their cellular distribution. Our results show that LPA-triggered regulatory pathways promote trophoblast endovascular response in vitro, suggesting a new role for LPA during spiral artery remodeling at the maternal-fetal interface.
dc.format application/pdf
dc.language.iso eng
dc.publisher Wiley-liss, Div John Wiley & Sons Inc
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject CYCLOOXYGENASE-2
dc.subject ENDOVASCULAR TROPHOBLAST
dc.subject INDUCIBLE NITRIC OXIDE SYNTHASE
dc.subject LPA3 RECEPTOR
dc.subject LYSOPHOSPHATIDIC ACID
dc.subject.classification Inmunología
dc.subject.classification Medicina Básica
dc.subject.classification CIENCIAS MÉDICAS Y DE LA SALUD
dc.title Lysophosphatidic acid-triggered pathways promote the acquisition of trophoblast endovascular phenotype in vitro
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2018-10-23T20:49:24Z
dc.journal.volume 119
dc.journal.number 1
dc.journal.pagination 758-772
dc.journal.pais Estados Unidos
dc.journal.ciudad New York
dc.description.fil Fil: Beltrame, Jimena Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
dc.description.fil Fil: Sordelli, Micaela Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
dc.description.fil Fil: Cañumil, Vanesa Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
dc.description.fil Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
dc.description.fil Fil: Ribeiro, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
dc.journal.title Journal of Cellular Biochemistry
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1002/jcb.26239
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.26239
dc.conicet.fuente Elsevier


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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)