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Vascular lipidomics analysis reveales increased levels of phosphocholine and lysophosphocholine in atherosclerotic mice

research-article

Author(s): Li Zhang ¹ ^, ² , Liling Xiong ¹ , Li Fan ¹ , Haoyang Diao ¹ , Mi Tang ¹ , Erdan Luo ¹ , Wenmei Guo ¹ , Xiao Yang ¹ ^, , Shasha Xing ¹ ^,

Publication date (Electronic): 4 January 2023

Journal: Nutrition & Metabolism

Publisher: BioMed Central

Keywords: Atherosclerosis, Untargeted lipidomics, ApoE−/− mice, Phosphocholines, Lysophosphocholines

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Abstract

Objective

Atherosclerosis (AS) is the major cause of cardiovascular disease, and dyslipidemia is a principal determinant of the initiation and progression of AS. Numerous works have analyzed the lipid signature of blood, but scarce information on the lipidome of vascular tissue is available. This study investigated the lipid profile in the aorta of ApoE ^−/− mice.

Method

ApoE ^−/− mice were randomly divided into two groups: (1) the normal diet (ND) group and (2) the high-fat diet (HFD) group. After feeding for 8 weeks, the plasma low-density lipoprotein (LDL), total cholesterol (TC), and triglyceride (TGs) levels were measured. UHPLC-Q Exactive plus MS was used to assess the lipid profile using both positive and negative ionization modes.

Results

LDL and TC levels were significantly increased in HFD mice, and lipid deposition, plaque area and collagen fiber levels were increased in HFD group. In addition, a total of 131 differential lipids were characterized, including 57 lipids with levels that were increased in the HFD group and 74 with levels that were decreased. Further analysis revealed that the levels of several differentially expressed phosphocholines (PCs) and lysophosphocholines (LPCs) were significantly increased. These PCs included PC (38:3), PC (36:4), PC (36:3), PC (36:2), PC (36:1), PC (34:1e), PC (34:1), PC (32:1), PC (18:0/18:1), and PC (38:5), and the LPCs included LPC (18:1), LPC (18:0) and LPC (16:0).

Conclusion

Our findings indicate the presence of a comprehensive lipid profile in the vascular tissue of atherosclerotic mice, particularly involving PC and LPC, which exhibited significantly increased levels in AS.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12986-022-00723-y.

Related collections

Most cited references 50

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Membrane lipids: where they are and how they behave.

Gerrit van Meer, Dennis Voelker, Gerald Feigenson (2008)

Throughout the biological world, a 30 A hydrophobic film typically delimits the environments that serve as the margin between life and death for individual cells. Biochemical and biophysical findings have provided a detailed model of the composition and structure of membranes, which includes levels of dynamic organization both across the lipid bilayer (lipid asymmetry) and in the lateral dimension (lipid domains) of membranes. How do cells apply anabolic and catabolic enzymes, translocases and transporters, plus the intrinsic physical phase behaviour of lipids and their interactions with membrane proteins, to create the unique compositions and multiple functionalities of their individual membranes?

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Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

Brian Ference, Henry N Ginsberg, Ian Graham … (2017)

Abstract Aims To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). Methods and results We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Conclusion Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

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Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis.

Michael Gimbrone, Guillermo García-Cardeña (2016)

Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Endothelial cell dysfunction, in its broadest sense, encompasses a constellation of various nonadaptive alterations in functional phenotype, which have important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox balance, and the orchestration of acute and chronic inflammatory reactions within the arterial wall. In this review, we trace the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explore its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerotic cardiovascular disease; consider current approaches to the clinical assessment of endothelial cell dysfunction; and outline some promising new directions for its early detection and treatment.

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Author and article information

Contributors

Xiao Yang: wcchgcptg@163.com

Shasha Xing: xingshasha1230@126.com

Journal

Journal ID (nlm-ta): Nutr Metab (Lond)

Journal ID (iso-abbrev): Nutr Metab (Lond)

Title: Nutrition & Metabolism

Publisher: BioMed Central (London )

ISSN (Electronic): 1743-7075

Publication date (Electronic): 4 January 2023

Publication date PMC-release: 4 January 2023

Publication date Collection: 2023

Volume: 20

Electronic Location Identifier: 1

Affiliations

[1 ]GRID grid.54549.39, ISNI 0000 0004 0369 4060, Chengdu Women’s and Children’s Central Hospital, School of Medicine, , University of Electronic Science and Technology of China, ; Chengdu, 611731 China

[2 ]GRID grid.16821.3c, ISNI 0000 0004 0368 8293, Hongqiao International Institute of Medicine, Tongren Hospital, , Shanghai Jiao Tong University School of Medicine, ; Shanghai, 200336 China

Article

Publisher ID: 723

DOI: 10.1186/s12986-022-00723-y

PMC ID: 9811766

PubMed ID: 36600244

SO-VID: c5812d01-92b5-42af-a1ac-8f52a51a4b52

Copyright © © The Author(s) 2023

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 4 October 2022

Date accepted : 30 December 2022

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 82201864

Award ID: 82100475

Award Recipient : Liling Xiong Shasha Xing

Categories

Subject: Research

Custom metadata

issue-copyright-statement © The Author(s) 2023

ScienceOpen disciplines: Nutrition & Dietetics

Keywords: atherosclerosis,untargeted lipidomics,apoe−/− mice,phosphocholines,lysophosphocholines

Data availability:

ScienceOpen disciplines: Nutrition & Dietetics

Keywords: atherosclerosis, untargeted lipidomics, apoe−/− mice, phosphocholines, lysophosphocholines

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