ArticleJournal of lipid research2012
Conformational changes of apoB-100 in SMase-modified LDL mediate formation of large aggregates at acidic pH.
Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- High cholesterol absorption efficiency enhances proatherogenic properties of low-density lipoprotein particles.Journal of internal medicine · 2026Article
- Cathelicidin LL-37-ApoB-100 interaction promotes LDL clearance and attenuates cholesterol accumulation in the liver.Science China. Life sciences · 2026Article
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
- Beyond cholesterol: linking the conformation of apolipoprotein B to atherogenesis.Current opinion in lipidology · 2025Review
- Apolipoprotein B-containing lipoproteins in atherogenesis.Nature reviews. Cardiology · 2025Review
- Sphingolipid metabolites involved in the pathogenesis of atherosclerosis: perspectives on sphingolipids in atherosclerosis.Cellular & molecular biology letters · 2025Review
- Emerging Roles for Sphingolipids in Cardiometabolic Disease: A Rational Therapeutic Target?Nutrients · 2024Review
- Article
- Effect of Sphingomyelinase-Treated LDLs on HUVECs.Molecules (Basel, Switzerland) · 2023Article
- Sphingolipids and Atherosclerosis: The Dual Role of Ceramide and Sphingosine-1-Phosphate.Antioxidants (Basel, Switzerland) · 2023Review
- Apolipoproteins as potential communicators play an essential role in the pathogenesis and treatment of early atherosclerosis.International journal of biological sciences · 2023Review
- Sphingolipids in Atherosclerosis: Chimeras in Structure and Function.International journal of molecular sciences · 2022Review
- Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis.Frontiers in cardiovascular medicine · 2022Review
- The Complex Tail of Circulating Sphingolipids in Atherosclerosis and Cardiovascular Disease.Journal of lipid and atherosclerosis · 2021Review
- Apolipoprotein and LRP1-Based Peptides as New Therapeutic Tools in Atherosclerosis.Journal of clinical medicine · 2021Review
- Aggregation Susceptibility of Low-Density Lipoproteins-A Novel Modifiable Biomarker of Cardiovascular Risk.Journal of clinical medicine · 2021Review
- Cysteamine inhibits lysosomal oxidation of low density lipoprotein in human macrophages and reduces atherosclerosis in mice.Atherosclerosis · 2019Article
- Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths.European heart journal · 2018Article
- ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker.Journal of cardiovascular development and disease · 2018Review
- A correlation between secondary structure and rheological properties of low-density lipoproteins at air/water interfaces.Journal of biological physics · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During atherogenesis, the extracellular pH of atherosclerotic lesions decreases. Here, we examined the effect of low, but physiologically plausible pH on aggregation of modified LDL, one of the key processes in atherogenesis. LDL was treated with SMase, and aggregation of the SMase-treated LDL was followed at pH 5.5-7.5. The lower the pH, the more extensive was the aggregation of identically prelipolyzed LDL particles. At pH 5.5-6.0, the aggregates were much larger (size >1 µm) than those formed at neutral pH (100-200 nm). SMase treatment was found to lead to a dramatic decrease in α-helix and concomitant increase in β-sheet structures of apoB-100. Particle aggregation was caused by interactions between newly exposed segments of apoB-100. LDL-derived lipid microemulsions lacking apoB-100 failed to form large aggregates. SMase-induced LDL aggregation could be blocked by lowering the incubation temperature to 15°C, which also inhibited the changes in the conformation of apoB-100, by proteolytic degradation of apoB-100 after SMase-treatment, and by HDL particles. Taken together, sphingomyelin hydrolysis induces exposure of protease-sensitive sites of apoB-100, whose interactions govern subsequent particle aggregation. The supersized LDL aggregates may contribute to the retention of LDL lipids in acidic areas of atherosclerosis-susceptible sites in the arterial intima.
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Registered trials
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.