ArticlePloS one2012
Postprandial apoE isoform and conformational changes associated with VLDL lipolysis products modulate monocyte inflammation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Linking alcohol use to Alzheimer's disease: Interactions with aging and APOE along immune pathways.Medical research archives · 2024Article
- iPSC-derived PSEN2 (N141I) astrocytes and microglia exhibit a primed inflammatory phenotype.Journal of neuroinflammation · 2024Article
- Apolipoprotein E4 has extensive conformational heterogeneity in lipid-free and lipid-bound forms.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Functional connectivity among brain regions affected in Alzheimer's disease is associated with CSF TNF-α in APOE4 carriers.Neurobiology of aging · 2020Article
- Article
- Inflammation: the link between comorbidities, genetics, and Alzheimer's disease.Journal of neuroinflammation · 2018Review
- Lipotoxic brain microvascular injury is mediated by activating transcription factor 3-dependent inflammatory and oxidative stress pathways.Journal of lipid research · 2016Article
- Associations between serum cholesterol levels and cerebral amyloidosis.JAMA neurology · 2014Article
- Binding of apolipoprotein E inhibits the oligomer growth of amyloid-β peptide in solution as determined by fluorescence cross-correlation spectroscopy.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
objectivePostprandial hyperlipemia, characterized by increased circulating very low-density lipoproteins (VLDL) and circulating lipopolysaccharide (LPS), has been proposed as a mechanism of vascular injury. Our goal was to examine the interactions between postprandial lipoproteins, LPS, and apoE3 and apoE4 on monocyte activation. METHODS AND
resultsWe showed that apoE3 complexed to phospholipid vesicles attenuates LPS-induced THP-1 monocyte cytokine expression, while apoE4 increases expression. ELISA revealed that apoE3 binds to LPS with higher affinity than apoE4. Electron paramagnetic resonance (EPR) spectroscopy of site-directed spin labels placed on specific amino acids of apoE3 showed that LPS interferes with conformational changes normally associated with lipid binding. Specifically, compared to apoE4, apoE bearing the E3-like R112→Ser mutation displays increased self association when exposed to LPS, consistent with a stronger apoE3-LPS interaction. Additionally, lipolysis of fasting VLDL from normal human donors attenuated LPS-induced TNFα secretion from monocytes to a greater extent than postprandial VLDL, an effect partially reversed by blocking apoE. This effect was reproduced using fasting VLDL lipolysis products from e3/e3 donors, but not from e4/e4 subjects, suggesting that apoE3 on fasting VLDL prevents LPS-induced inflammation more readily than apoE4.
conclusionPostprandial apoE isoform and conformational changes associated with VLDL dramatically modulate vascular inflammation.
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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 OpenQuestion graph.