ArticleLipids in health and disease2016
APOC3 induces endothelial dysfunction through TNF-α and JAM-1.
Article in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 30 citations in OpenAlex.
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- The role of cell junctions in atherosclerosis: implications for inflammation, endothelial dysfunction, and plaque stability.Journal of physiology and biochemistry · 2025Review
- Increased serum APOC3 in patients with syphilis can predict the absence of Jarisch-Herxheimer reaction after benzathine penicillin treatment.Journal of the Chinese Medical Association : JCMA · 2025Article
- ApoC-III proteoforms are associated with better lipid, inflammatory, and glucose profiles independent of total apoC-III.Cardiovascular diabetology · 2024Article
- New approaches to triglyceride reduction: Is there any hope left?American journal of preventive cardiology · 2024Article
- CD14International journal of molecular sciences · 2023Article
- Interventional hepatic apoC-III knockdown improves atherosclerotic plaque stability and remodeling by triglyceride lowering.JCI insight · 2022Article
- Plasma Proteome Profiling of Patients With In-stent Restenosis by Tandem Mass Tag-Based Quantitative Proteomics Approach.Frontiers in cardiovascular medicine · 2022Article
- Apolipoprotein C-III and cardiovascular diseases: when genetics meet molecular pathologies.Molecular biology reports · 2021Review
- Association between Genetic Variant ofNutrients · 2018Article
- Thymoquinone reduces cardiac damage caused by hypercholesterolemia in apolipoprotein E-deficient mice.Lipids in health and disease · 2018Article
- Hypertriglyceridemia and atherosclerosis.Lipids in health and disease · 2017Review
- The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Reduces Aortic Damage from Hypercholesterolaemia in Apolipoprotein E-Deficient Mice.Biomedicine hubArticle
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe fatality rate for cardiovascular disease (CVD) has increased in recent years and higher levels of triglyceride have been shown to be an independent risk factor for atherosclerotic CVD. Dysfunction of endothelial cells (ECs) is also a key factor of CVD. APOC3 is an important molecule in lipid metabolism that is closely associated with hyperlipidemia and an increased risk of developing CVD. But the direct effects of APOC3 on ECs were still unknown. This study was aimed at determining the effects of APOC3 on inflammation, chemotaxis and exudation in ECs.
methodsELISA, qRT-PCR, immunofluorescence, flow cytometry and transwell assays were used to investigate the effects of APOC3 on human umbilical vein endothelial cells (HUVECs). SiRNA-induced TNF-α and JAM-1 silencing were used to observe how APOC3 influenced the inflammatory process in the ECs.
resultsOur results showed that APOC3 was closely associated with the inflammatory process in ECs, and that this process was characterized by the increased expression of TNF-α. Inflammatory processes further disrupted the tight junctions (TJs) between HUVECs by causing increased expression of JAM-1. JAM-1 was involved in maintaining the integrity of TJs, and it promoted the assembly of platelets and the exudation of leukocytes. Changes in its expression promoted chemotaxis and the exudation of ECs, which contributed to atherosclerosis. While the integrity of the TJs was disrupted, the adhesion of THP-1 cells to HUVECs was also increased by APOC3.
conclusionsIn this study, we describe the mechanism by which APOC3 causes inflammation, chemotaxis and the exudation of ECs, and we suggest that controlling the inflammatory reactions that are caused by APOC3 may be a new method to treat CVD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.