Lipid Remodeling in Mouse SR-B1-Deficient Embryos with Oxidative Stress-Associated Neural Tube Defects.

Overview

1. Ph.D. Program in Medical Science, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile
2. Institute of Health Sciences, Universidad de O’Higgins, Rancagua 2820000, Chile
3. Great Ormond Street Institute of Child Health, University College London, London WC1N 1EH, UK
4. Biomedical Research and Innovation Center, Faculty of Medicine, Universidad de Los Andes, Santiago 7550000, Chile
5. Center of Interventional Medicine for Precision and Advanced Cellular Therapy (IMPACT), Santiago 7550000, Chile

Abstract

Neural tube defects (NTD) are congenital malformations that lead to structural abnormalities of the brain or spine. Mouse embryos deficient in Scavenger Receptor Class B Type 1 (SR-B1 KO), the main receptor for high-density lipoproteins, exhibit a high incidence of anterior NTD, which is associated with vitamin E deficiency and elevated levels of reactive oxygen species (ROS). Maternal supplementation with vitamin E, a micronutrient with antioxidant properties, completely prevents the occurrence of NTD and normalizes ROS levels in SR-B1 KO embryos, suggesting a contribution of oxidative stress to NTD in this model. In this work, we showed that SR-B1 KO embryos at gestational day E9.5 display higher levels of lipoperoxidative damage markers. Analysis of data obtained through shotgun lipidomics evidenced a selective and coordinated reorganization of fatty acid distribution, characterized by altered polyunsaturated and monounsaturated composition, together with reduced phosphatidylcholine and increased lysophosphatidylcholine levels, and diversion of fatty acids into triacylglyceride storage. Transcriptomic analysis revealed a coordinated upregulation of genes involved in phospholipid synthesis and remodeling, consistent with the altered lipid homeostasis observed in SR-B1 KO embryos. Together, these results provide novel information showing a potential link between oxidative stress and disruptions in mammalian embryonic lipid metabolism, highlighting phospholipid remodeling as a potential determinant of susceptibility to NTD.

Reproduced under the paper's license (CC BY), from the paper cited above.

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Data

Datasets cited

• geo:GSE115091, at NCBI GEO; found in “Data Availability Statement”

Data Availability Statement

The original contributions presented in this study are included in the Supplementary Material. Further inquires can be directed to the corresponding author. The transcriptomic data generated in a previous study and analyzed in this paper are publicly available in the Gene Expression Omnibus (GEO) repository under accession number GSE115091 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115091).

Reproduced under the paper's license (CC BY), from the paper cited above.

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Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 5 authors, 5 keywords, 2 funders, 73 references.

Cite

This paper

Quiroz, A., Santander, N., Nicolás, G. D. E., Leung, K.-Y., & Busso, D. (2026). Lipid Remodeling in Mouse SR-B1-Deficient Embryos with Oxidative Stress-Associated Neural Tube Defects. Antioxidants (Basel, Switzerland), 15(5), 634. https://doi.org/10.3390/antiox15050634

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