Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells
Abstract
Background Lipoproteins containing apolipoprotein (apo) CIII predict coronary heart disease and associate with components of the metabolic syndrome. ApoCIII inhibits lipoprotein catabolism in plasma. However, it is unknown whether apoCIII itself, or in association with VLDL, LDL, or HDL, directly affects atherogenic mechanisms in vascular cells. Thus, we investigated the direct effect of lipoproteins that do or do not have apoCIII, and apoCIII itself, on adhesion of THP-1 cells, a human monocytic cell line, to vascular endothelial cells (ECs). Methods and results VLDL CIII+ and LDL CIII+ (100 microg apoB/mL) from fasting plasma of 18 normolipidemic volunteers increased THP-1 cell adhesion to ECs under static conditions by 2.4+/-0.3-fold and 1.8+/-0.7-fold, respectively (P Conclusions ApoB lipoproteins that contain apoCIII increase THP-1 cell adhesion to ECs via PKCalpha and RhoA-mediated beta1-integrin activation. These results indicate that apoCIII not only modulates lipoprotein metabolism but also may directly contribute to the development of atherosclerosis.
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VLDL and LDL particles carrying APOC-III-but not those lacking APOC-III-initiate atherosclerosis by promoting endothelial injury and monocyte adhesion.
“Moreover, VLDL and LDL particles carrying APOC-III—but not those lacking APOC-III—initiate atherosclerosis by promoting endothelial injury and monocyte adhesion [28, 29].”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [28]
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“Moreover, VLDL and LDL particles carrying APOC-III—but not those lacking APOC-III—initiate atherosclerosis by promoting endothelial injury and monocyte adhesion [28, 29].”
- Authors
- Kawakami, A., Aikawa, M., Libby, P., Alcaide, P., Luscinskas, F. W., & Sacks, F. M.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- Circulation
- Published
- 2006-02-07
- Volume
- 113
- Issue
- 5
- Pages
- 691-700
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2138061818
- Cited by
- 206
- References
- 6
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 9 · 2023: 8 · 2022: 10 · 2021: 11 · 2020: 12 · 2019: 7 · 2018: 7 · 2017: 6 · 2016: 9 · 2015: 11 · 2014: 10 · 2013: 14 · 2012: 11
- FWCI
- 4.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Donald W. Reynolds Foundation
- National Heart, Lung, and Blood Institute (P50HL056985, HL-80472, R01HL069376, HL53393, HL69376, HL56985, P01HL036028, R01HL080472, HL36028, HL-48743, P01HL048743)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- apolipoprotein C-III, VLDL, low-density lipoprotein, HDL cholesterol, THP-1 cells, endothelial cells, shear flow, protein kinase C alpha, RhoA, β1 integrin activation, atherosclerosis, coronary artery disease, metabolic syndrome
- MeSH terms
- Apolipoproteins B, Apolipoproteins C, Cell Adhesion, Endothelium, Vascular, Humans, Lipoproteins, Lipoproteins, LDL, Lipoproteins, VLDL, Monocytes, Integrin beta1, rhoA GTP-Binding Protein, Atherosclerosis, Protein Kinase C-alpha, Apolipoprotein C-III
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