Deficient Vitamin E Uptake during Development Impairs Neural Tube Closure in Mice Lacking Lipoprotein Receptor SR-BI

Nicolás Santander, Carlos Lizama, María José Parga, Alonso Quiroz, Druso Pérez, Guadalupe Echeverría, Lorena Ulloa, Verónica Palma, Attilio Rigotti, Dolores Busso

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

SR-BI is the main receptor for high density lipoproteins (HDL) and mediates the bidirectional transport of lipids, such as cholesterol and Vitamin E, between these particles and cells. During early development, SR-BI is expressed in extraembryonic tissue, specifically in trophoblast giant cells in the parietal yolk sac. We previously showed that approximately 50% of SR-BI-/- embryos fail to close the anterior neural tube and develop exencephaly, a perinatal lethal condition. Here, we evaluated the role of SR-BI in embryonic Vitamin E uptake during murine neural tube closure. Our results showed that SR-BI-/- embryos had a very low Vitamin E content in comparison to SR-BI+/+ embryos. Whereas SR-BI-/- embryos with closed neural tubes (nSR-BI-/-) had high levels of reactive oxygen species (ROS), intermediate ROS levels between SR-BI+/+ and nSR-BI-/- embryos were detected in SR-BI-/- with NTD (NTD SR-BI-/-). Reduced expression of Pax3, Alx1 and Alx3 genes was found in NTD SR-BI-/- embryos. Maternal α-tocopherol dietary supplementation prevented NTD almost completely (from 54% to 2%, p < 0.001) in SR-BI-/- embryos and normalized ROS and gene expression levels. In sum, our results suggest the involvement of SR-BI in the maternal provision of embryonic Vitamin E to the mouse embryo during neural tube closure.

Original languageEnglish
Article number5182
JournalScientific Reports
Volume7
Issue number1
DOIs
StatePublished - 1 Dec 2017
Externally publishedYes

Bibliographical note

Funding Information:
This study was financed by the Chilean National Council for Scientific and Technological Research (CONICYT) programs Fondo Nacional del Desarrollo Cient?fico y Tecnol?gico (FONDECYT) no. 1141236 (to D.B.), no. 1150399 (to A.R.), no. 1140697 (to V.P.), Ph.D. Fellowship no. 21130444 (to N.S.) and the School of Medicine grant PMD-04/16 (to N.S.).

Publisher Copyright:
© 2017 The Author(s).

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