Low-density lipoprotein modified by myeloperoxidase oxidants induces endothelial dysfunction
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Low-density lipoprotein (LDL) modified by hypochlorous acid (HOCl) produced by myeloperoxidase (MPO) is present in atherosclerotic lesions, where it is implicated in the propagation of inflammation and acceleration of lesion development by multiple pathways, including the induction of endothelial dysfunction . Thiocyanate (SCN - ) ions are utilised by MPO to produce the oxidant hypothiocyanous acid (HOSCN), which reacts with LDL in a different manner to HOCl. Whilst the reactivity of HOCl-modified LDL has been previously studied, the role of HOSCN in the modification of LDL in vivo is poorly defined, although emerging evidence suggests that these particles have distinct biological properties. This is important because elevated plasma SCN - is linked with both the propagation and prevention of atherosclerosis . In this study, we demonstrate that both HOSCN- and HOCl-modified LDL inhibit endothelium-mediated vasorelaxation ex vivo in rat aortic ring segments. In vitro experiments with human coronary artery endothelial cells show that HOSCN-modified LDL decreases in the production of nitric oxide (NO • ) and induces the loss of endothelial nitric oxide synthase (eNOS) activity. This occurs to a similar extent to that seen with HOCl-modified LDL. In each case, these effects are related to eNOS uncoupling, rather than altered expression, phosphorylation or cellular localisation . Together, these data provide new insights into role of MPO and LDL modification in the induction of endothelial dysfunction, which has implications for both the therapeutic use of SCN - within the setting of atherosclerosis and for smokers, who have elevated plasma levels of SCN - , and are more at risk of developing cardiovascular disease.
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HOCl decreases eNOS activity and NO bioavailability by a number of direct and indirect mechanisms, disrupting protective NO signaling.
“Hypochlorous acid decreases eNOS activity and NO bioavailability by a number of direct and indirect mechanisms, disrupting protective NO signaling (2, 464, 1054).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [2]
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- Authors
- Abdo, A. I., Rayner, B. S., van Reyk, D. M., & Hawkins, C. L.
- Affiliations
- The University of Sydney (AU)
- University of Copenhagen (DK)
- Corresponding author
- Hawkins, Clare L.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 13
- Pages
- 623-632
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC5558469
- OpenAlex
- W2745305461
- Cited by
- 51
- References
- 62
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 3 · 2023: 6 · 2022: 7 · 2021: 8 · 2020: 6 · 2019: 7 · 2018: 2
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UTS ePRESS (University of Technology Sydney) (submittedVersion)
- Funders
- University of Sydney
- Australian Research Council (FT120100682)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- LDL oxidation, myeloperoxidase, hypochlorous acid, hypothiocyanous acid, thiocyanate, endothelial dysfunction, nitric oxide, endothelial nitric oxide synthase uncoupling, atherosclerosis, vasorelaxation, smokers
- MeSH terms
- Animals, Aorta, Cells, Cultured, Hypochlorous Acid, Lipoproteins, LDL, Male, Peroxidase, Nitric Oxide, Thiocyanates, Vasodilation, Rats, Sprague-Dawley, Endothelial Cells, Rats, Nitric Oxide Synthase Type III
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