ArticlePloS one2013
Apolipoprotein A-I glycation by glucose and reactive aldehydes alters phospholipid affinity but not cholesterol export from lipid-laden macrophages.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- HDL metabolism and function in diabetes mellitus.Nature reviews. Endocrinology · 2026Review
- A Study on Multiple Facets of Apolipoprotein A1 Milano.Applied biochemistry and biotechnology · 2023Review
- Cardiovascular Disease in South Asian Immigrants: a Review of Dysfunctional HDL as a Potential Marker.Journal of racial and ethnic health disparities · 2023Review
- The Glyoxalase System Is a Novel Cargo of Amniotic Fluid Stem-Cell-Derived Extracellular Vesicles.Antioxidants (Basel, Switzerland) · 2022Article
- Resolution of apolipoprotein A1 and A2 proteoforms: their cardiometabolic correlates and implications for future research.Current opinion in lipidology · 2022Review
- High Density Lipoproteins and Diabetes.Cells · 2021Review
- A misprocessed form of Apolipoprotein A-I is specifically associated with recurrent Focal Segmental Glomerulosclerosis.Scientific reports · 2020Article
- Advanced Glycated apoA-IV Loses Its Ability to Prevent the LPS-Induced Reduction in Cholesterol Efflux-Related Gene Expression in Macrophages.Mediators of inflammation · 2020Article
- The Role of High-Density Lipoproteins in Diabetes and Its Vascular Complications.International journal of molecular sciences · 2018Review
- A Targeted, Differential Top-Down Proteomic Methodology for Comparison of ApoA-I Proteoforms in Individuals with High and Low HDL Efflux Capacity.Journal of proteome research · 2018Article
- Glycation Reduces the Stability of ApoAI and Increases HDL Dysfunction in Diet-Controlled Type 2 Diabetes.The Journal of clinical endocrinology and metabolism · 2018Article
- Cholesterol Efflux Capacity of Apolipoprotein A-I Varies with the Extent of Differentiation and Foam Cell Formation of THP-1 Cells.Journal of lipids · 2016Article
- Residual Cardiovascular Risk in Chronic Kidney Disease: Role of High-density Lipoprotein.Archives of medical research · 2015Review
- Biomarkers associated with high-density lipoproteins in atherosclerotic kidney disease.Clinical and experimental nephrology · 2014Review
- Top-down proteomics of a drop of blood for diabetes monitoring.Journal of proteome research · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased protein glycation in people with diabetes may promote atherosclerosis. This study examined the effects of non-enzymatic glycation on the association of lipid-free apolipoproteinA-I (apoA-I) with phospholipid, and cholesterol efflux from lipid-loaded macrophages to lipid-free and lipid-associated apoA-I. Glycation of lipid-free apoA-I by methylglyoxal and glycolaldehyde resulted in Arg, Lys and Trp loss, advanced glycation end-product formation and protein cross-linking. The association of apoA-I glycated by glucose, methylglyoxal or glycolaldehyde with phospholipid multilamellar vesicles was impaired in a glycating agent dose-dependent manner, with exposure of apoA-I to both 30 mM glucose (42% decrease in kslow) and 3 mM glycolaldehyde (50% decrease in kfast, 60% decrease in kslow) resulting is significantly reduced affinity. Cholesterol efflux to control or glycated lipid-free apoA-I, or discoidal reconstituted HDL containing glycated apoA-I (drHDL), was examined using cholesterol-loaded murine (J774A.1) macrophages treated to increase expression of ATP binding cassette transporters A1 (ABCA1) or G1 (ABCG1). Cholesterol efflux from J774A.1 macrophages to glycated lipid-free apoA-I via ABCA1 or glycated drHDL via an ABCG1-dependent mechanism was unaltered, as was efflux to minimally modified apoA-I from people with Type 1 diabetes, or controls. Changes to protein structure and function were prevented by the reactive carbonyl scavenger aminoguanidine. Overall these studies demonstrate that glycation of lipid-free apoA-I, particularly late glycation, modifies its structure, its capacity to bind phospholipids and but not ABCA1- or ABCG1-dependent cholesterol efflux from macrophages.
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Registered trials
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