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      Low Very low-Density Lipoprotein Cholesterol but High Very low-Density Lipoprotein Receptor mRNA Expression in Peripheral White Blood Cells: An Atherogenic Phenotype for Atherosclerosis in a Community-Based Population ☆

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          Abstract

          Very low-density lipoprotein cholesterol (VLDL-C), via binding very low-density lipoprotein receptor (VLDLR), can induce the development of atherosclerosis. Besides monocytes, VLDLR expression is detected in various peripheral white blood cells (WBCs), yet its underlying role remains unclear. We thereby aimed to test the hypothesis that VLDLR in all types of peripheral WBCs may be involved in the association between VLDL-C and atherosclerosis. VLDLR mRNA expression in peripheral WBC and plasma VLDL-C levels were measured in 747 participants from a community-based study. Plaque prevalence and total plaque area (TPA) were used to evaluate the burden of carotid atherosclerosis. VLDL-C was positively associated with atherosclerosis risk, whereas this association was modified by VLDLR mRNA level. In participants with the lowest VLDL-C but the highest VLDLR mRNA expression, the risk for plaque prevalence unexpectedly was the highest. This association was also observed for TPA. Moreover, this association remained unchanged after adjusting for WBC or monocytes. Our findings described an atherogenic phenotype characterized by low VLDL-C but high VLDLR mRNA expression in peripheral WBCs, which suggested that VLDLR in all types of peripheral WBCs may be involved in lipid deposition, and VLDL-C and VLDLR may co-determine the development of atherosclerosis.

          Highlights

          • •

            VLDL-C level is one of risk factors for atherosclerosis.

          • •

            The risk of carotid atherosclerosis increased higher among participants with low VLDL-C but high VLDLR mRNA expression.

          • •

            VLDLR in all types of peripheral WBCs was involved in lipid deposition.

          • •

            VLDL-C and VLDLR may co-determine the divergent degree of atherosclerotic cardiovascular disease risk.

          Very low-density lipoprotein (VLDL), via binding VLDL receptor can induce the development of atherosclerosis. VLDL receptor expression is detected in various peripheral WBCs yet its underlying role remains unclear. Our findings suggested that VLDL cholesterol is an independent risk factor for atherosclerosis. Participants with low levels of VLDL cholesterol, from being in a lower cardiovascular risk, yet increased risk if combined with high VLDLR mRNA expression in peripheral WBCs, indicating the focus of future intervention studies should therefore on decreasing VLDL cholesterol and VLDL receptor expression, and investigating the mechanisms of receptor-mediated atherogenic processes in all types of peripheral WBCs.

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          Carotid plaque area: a tool for targeting and evaluating vascular preventive therapy.

          T Lohmann, Maria DiCicco, Dan Hackam … (2002)
          Carotid plaque area measured by ultrasound (cross-sectional area of longitudinal views of all plaques seen) was studied as a way of identifying patients at increased risk of stroke, myocardial infarction, and vascular death. Patients from an atherosclerosis prevention clinic were followed up annually for up to 5 years (mean, 2.5+/-1.3 years) with baseline and follow-up measurements recorded. Plaque area progression (or regression) was defined as an increase (or decrease) of >/=0.05 cm(2) from baseline. Carotid plaque areas from 1686 patients were categorized into 4 quartile ranges: 0.00 to 0.11 cm(2) (n=422), 0.12 to 0.45 cm(2) (n=424), 0.46 to 1.18 cm(2) (n=421), and 1.19 to 6.73 cm(2) (n=419). The combined 5-year risk of stroke, myocardial infarction, and vascular death increased by quartile of plaque area: 5.6%, 10.7%, 13.9%, and 19.5%, respectively (P /=1 annual carotid plaque area measurements: 685 (63.1%) had carotid plaque progression, 306 (28.2%) had plaque regression, and 176 (16.2%) had no change in carotid plaque area over the period of follow-up. The 5-year adjusted risk of combined outcome was 9.4%, 7.6%, and 15.7% for patients with carotid plaque area regression, no change, and progression, respectively (P=0.003). Carotid plaque area and progression of plaque identified high-risk patients. Plaque measurement may be useful for targeting preventive therapy and evaluating new treatments and response to therapy and may improve cost-effectiveness of secondary preventive treatment.
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            Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL.

            Miguel A. Lasunción, Elkin Y. Suárez-Villota, D Calvo … (1998)
            Mouse and hamster SR-BI glycoproteins and their putative human counterpart CLA-I are so far the only scavenger receptors known to bind both native and modified lipoproteins. CD36, a multigland glycoprotein structurally related to SR-BI and CLA-1, has been reported to bind oxidized low density lipoprotein (OxLDL) and acetylated LDL (AcLDL). In this report, we have studied the ability of CD36 to bind native lipoproteins. By transient expression of human CD36 in mammalian and insect cells, we demonstrate that CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, VLDL, and, as previously reported, for OxLDL and AcLDL. The specificity of these interactions is supported by the dose-dependent inhibiton, effect of a monoclonal antibody against CD36. Furthermore, at least for HDL, binding to CD36 does not require the presence of apoE. These findings, together with preferential expression of CD36 in tissues performing very active fatty acid metabolism (skeletal muscle, heart, mammary epithelium, and adipose tissue) and its involvement in foam cell formation (macrophages), suggest that binding of lipoproteins to CD36 might contribute to the regulation of lipid metabolism, and to the pathogenesis of atherosclerosis.
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              Non-high-density lipoprotein and very-low-density lipoprotein cholesterol and their risk predictive values in coronary heart disease.

              Maurizio Trevisan, Christopher T. Sempos, Scott M. Grundy … (2006)
              To determine if non-high-density lipoprotein (HDL) cholesterol is a more useful predictor of coronary heart disease (CHD) risk than low-density lipoprotein (LDL) cholesterol and if very-low-density lipoprotein (VLDL) cholesterol is an independent predictor of CHD risk, data from the Framingham Heart Study (2,693 men, 3,101 women) were used for this analysis. All subjects were aged > or =30 years and free of CHD at baseline, and incident CHD was the end point (618 men, 372 women). Cox proportional-hazards models were used to assess the risk for CHD (relative risks and 95% confidence intervals) on the basis of the joint distribution of LDL cholesterol and non-HDL cholesterol (in milligrams per deciliter), as well as LDL cholesterol, non-HDL cholesterol, and VLDL cholesterol as continuous variables. After multivariate adjustment, within non-HDL cholesterol level, no association was found between LDL cholesterol and the risk for CHD, whereas within LDL cholesterol levels, a strong positive and graded association between non-HDL cholesterol and risk for CHD was observed. When the analysis was repeated within triglyceride levels ( or =200 mg/dl), the risk pattern did not change significantly. Also, VLDL cholesterol was found to be a significant predictor of CHD risk after adjusting for LDL cholesterol at triglyceride levels of > or =200 or <200 mg/dl. In conclusion, these results suggest that non-HDL cholesterol level is a stronger predictor of CHD risk than LDL cholesterol; that is, VLDL cholesterol may play a critical role in the development of CHD.
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                Author and article information

                Contributors
                Yue Qi
                Journal
                Journal ID (nlm-ta): EBioMedicine
                Journal ID (iso-abbrev): EBioMedicine
                Title: EBioMedicine
                Publisher: Elsevier
                ISSN (Electronic): 2352-3964
                Publication date PMC-release: 31 August 2017
                Publication date Collection: November 2017
                Publication date (Electronic): 31 August 2017
                Volume: 25
                Pages: 136-142
                Affiliations
                Department of Epidemiology, Beijing An Zhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China
                Author notes
                [* ]Corresponding author at: Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, No. 2 An Zhen Road, Chaoyang District, Beijing 100029, China.Beijing An Zhen HospitalCapital Medical UniversityBeijing Institute of Heart, Lung and Blood Vessel DiseasesNo. 2 An Zhen RoadChaoyang DistrictBeijing100029China qiyue_bjcn@ 123456163.com
                Article
                Publisher ID: S2352-3964(17)30336-5
                DOI: 10.1016/j.ebiom.2017.08.019
                PMC ID: 5704045
                PubMed ID: 29042132
                SO-VID: 3537969b-87c4-4488-9ad4-4aa77ca10cbc
                Copyright © © 2017 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 6 June 2017
                Date revision received : 15 August 2017
                Date accepted : 21 August 2017
                Categories
                Subject: Research Paper

                Keywords: very low-density lipoprotein cholesterol,very low-density lipoprotein receptor,carotid atherosclerosis,community-based study
                Data availability:
                Keywords: very low-density lipoprotein cholesterol, very low-density lipoprotein receptor, carotid atherosclerosis, community-based study

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