Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature

Abstract Maternal physiological or supraphysiological hypercholesterolemia (MPH, MSPH) occurs during pregnancy. MSPH is associated with foetal endothelial dysfunction and atherosclerosis. However, the potential effects of MSPH on placental microvasculature are unknown. The aim of this study was to d...

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Autores principales:	Bárbara Fuenzalida, Bastián Sobrevia, Claudette Cantin, Lorena Carvajal, Rocío Salsoso, Jaime Gutiérrez, Susana Contreras-Duarte, Luis Sobrevia, Andrea Leiva
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/92e3d8311e574861ae55e15e21938819
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spelling	oai:doaj.org-article:92e3d8311e574861ae55e15e219388192021-12-02T11:41:03ZMaternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature10.1038/s41598-018-25985-62045-2322https://doaj.org/article/92e3d8311e574861ae55e15e219388192018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25985-6https://doaj.org/toc/2045-2322Abstract Maternal physiological or supraphysiological hypercholesterolemia (MPH, MSPH) occurs during pregnancy. MSPH is associated with foetal endothelial dysfunction and atherosclerosis. However, the potential effects of MSPH on placental microvasculature are unknown. The aim of this study was to determine whether MSPH alters endothelial function in the placental microvasculature both ex vivo in venules and arterioles from the placental villi and in vitro in primary cultures of placental microvascular endothelial cells (hPMEC). Total cholesterol < 280 mg/dL indicated MPH, and total cholesterol ≥280 mg/dL indicated MSPH. The maximal relaxation to histamine, calcitonin gene-related peptide and adenosine was reduced in MSPH venule and arteriole rings. In hPMEC from MSPH placentas, nitric oxide synthase (NOS) activity and L-arginine transport were reduced without changes in arginase activity or the protein levels of endothelial NOS (eNOS), human cationic amino acid 1 (hCAT-1), hCAT-2A/B or arginase II compared with hPMEC from MPH placentas. In addition, it was shown that adenosine acts as a vasodilator of the placental microvasculature and that NOS is active in hPMEC. We conclude that MSPH alters placental microvascular endothelial function via a NOS/L-arginine imbalance. This work also reinforces the concept that placental endothelial cells from the macro- and microvasculature respond differentially to the same pathological condition.Bárbara FuenzalidaBastián SobreviaClaudette CantinLorena CarvajalRocío SalsosoJaime GutiérrezSusana Contreras-DuarteLuis SobreviaAndrea LeivaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bárbara Fuenzalida Bastián Sobrevia Claudette Cantin Lorena Carvajal Rocío Salsoso Jaime Gutiérrez Susana Contreras-Duarte Luis Sobrevia Andrea Leiva Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
description	Abstract Maternal physiological or supraphysiological hypercholesterolemia (MPH, MSPH) occurs during pregnancy. MSPH is associated with foetal endothelial dysfunction and atherosclerosis. However, the potential effects of MSPH on placental microvasculature are unknown. The aim of this study was to determine whether MSPH alters endothelial function in the placental microvasculature both ex vivo in venules and arterioles from the placental villi and in vitro in primary cultures of placental microvascular endothelial cells (hPMEC). Total cholesterol < 280 mg/dL indicated MPH, and total cholesterol ≥280 mg/dL indicated MSPH. The maximal relaxation to histamine, calcitonin gene-related peptide and adenosine was reduced in MSPH venule and arteriole rings. In hPMEC from MSPH placentas, nitric oxide synthase (NOS) activity and L-arginine transport were reduced without changes in arginase activity or the protein levels of endothelial NOS (eNOS), human cationic amino acid 1 (hCAT-1), hCAT-2A/B or arginase II compared with hPMEC from MPH placentas. In addition, it was shown that adenosine acts as a vasodilator of the placental microvasculature and that NOS is active in hPMEC. We conclude that MSPH alters placental microvascular endothelial function via a NOS/L-arginine imbalance. This work also reinforces the concept that placental endothelial cells from the macro- and microvasculature respond differentially to the same pathological condition.
format	article
author	Bárbara Fuenzalida Bastián Sobrevia Claudette Cantin Lorena Carvajal Rocío Salsoso Jaime Gutiérrez Susana Contreras-Duarte Luis Sobrevia Andrea Leiva
author_facet	Bárbara Fuenzalida Bastián Sobrevia Claudette Cantin Lorena Carvajal Rocío Salsoso Jaime Gutiérrez Susana Contreras-Duarte Luis Sobrevia Andrea Leiva
author_sort	Bárbara Fuenzalida
title	Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
title_short	Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
title_full	Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
title_fullStr	Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
title_full_unstemmed	Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
title_sort	maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/92e3d8311e574861ae55e15e21938819
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Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature

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