Transfer and Enzyme-Mediated Metabolism of Oxidized Phosphatidylcholine and Lysophosphatidylcholine between Low- and High-Density Lipoproteins

Sawada, Naruhiko; Obama, Takashi; Mizuno, Mirei; Fukuhara, Kiyoshi; Iwamoto, Satoshi; Aiuchi, Toshihiro; Makiyama, Tomohiko; Itabe, Hiroyuki

doi:10.3390/antiox9111045

Cited by 14 publications

(15 citation statements)

References 34 publications

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“…LDL containing [ 2 H]-labeled 1-palmitoyl-lysoPC was incubated with HDL for up to 4 h, then [ 2 H]-labeled lipids in the LDL and HDL fractions were monitored using LC-MS/MS. Under these conditions, lysoPC in LDL was decreased during the incubation, while newly formed diacyl-PC in both LDL and HDL fractions increased concomitantly [106]. The production of diacyl-PC was abolished by an LCAT inhibitor.…”

Section: Oxpc Metabolism In the Presence Of Hdlmentioning

confidence: 90%

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

et al. 2021

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Oxidative modification of lipoproteins is implicated in the occurrence and development of atherosclerotic lesions. Earlier studies have elucidated on the mechanisms of foam cell formation and lipid accumulation in these lesions, which is mediated by scavenger receptor-mediated endocytosis of oxidized low-density lipoprotein (oxLDL). Mounting clinical evidence has supported the involvement of oxLDL in cardiovascular diseases. High-density lipoprotein (HDL) is known as anti-atherogenic; however, recent studies have shown circulating oxidized HDL (oxHDL) is related to cardiovascular diseases. A modified structure of oxLDL, which was increased in the plasma of patients with acute myocardial infarction, was characterized. It had two unique features: (1) a fraction of oxLDL accompanied oxHDL, and (2) apoA1 was heavily modified, while modification of apoB, and the accumulation of oxidized phosphatidylcholine (oxPC) and lysophosphatidylcholine (lysoPC) was less pronounced. When LDL and HDL were present at the same time, oxidized lipoproteins actively interacted with each other, and oxPC and lysoPC were transferred to another lipoprotein particle and enzymatically metabolized rapidly. This brief review provides a novel view on the dynamics of oxLDL and oxHDL in circulation.

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Section: Oxpc Metabolism In the Presence Of Hdlmentioning

confidence: 90%

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

et al. 2021

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“…[ 32 ] Subsequently, it is plausible to be oxidized by free radicals and modified to form ox‐LDL. [ 33 ] The continuous accumulation of ox‐LDL triggers the innate inflammatory response within the intima, stimulates activated ECs to express adhesion molecules such as vascular cell adhesion molecule‐1 (VCAM‐1) and intracellular adhesion molecule‐1, and induces the release of chemotactic molecules (e.g., monocyte chemotactic protein‐1 (MCP‐1)) in VSMCs, which together recruit monocytes and lymphocytes into the subendothelial space. [ 34 ] Then, monocytes differentiate into macrophages under the regulation of macrophage colony‐stimulating factor.…”

Section: The Development Of Atherosclerosis and Pathological Characte...mentioning

confidence: 99%

Targeting the Microenvironment of Vulnerable Atherosclerotic Plaques: An Emerging Diagnosis and Therapy Strategy for Atherosclerosis

et al. 2022

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Atherosclerosis is considered one of the primary causes of cardiovascular diseases (CVDs). Unpredictable rupture of the vulnerable atherosclerotic plaques triggers adverse cardiovascular events such as acute myocardial syndrome and even sudden cardiac death. Therefore, assessing the vulnerability of atherosclerotic plaques and early intervention are of significance in reducing CVD mortality. Nanomedicine possesses tremendous advantages in achieving the integration of the diagnosis and therapy of atherosclerotic plaques because of its magnetic, optical, thermal, and catalytic properties. Based on the pathological characteristics of vulnerable plaques, stimuli‐responsive nanoplatforms and surface‐functionalized nanoagents are designed and have drawn great attention for accomplishing the precise imaging and treatment of vulnerable atherosclerotic plaques due to their superior properties, such as high bioavailability, lesion‐targeting specificity, on‐demand cargo release, and low off‐target damage. Here, the characteristics of vulnerable plaques are generalized, and some targeted strategies for boosting the accuracy of plaque vulnerability evaluation by imaging and the efficacy of plaque stabilization therapy (including antioxidant therapy, macrophage depletion therapy, regulation of lipid metabolism therapy, anti‐inflammation therapy, etc.) are systematically summarized. In addition, existing challenges and prospects in this field are discussed, and it is believed to provide new thinking for the diagnosis and treatment of CVDs in the near future.

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“…Upon OxLDL clearance, engulfing macrophages are converted into foam cells -hallmark cells of atherosclerotic plaques (28)(29)(30). Additionally, MDA-, 4-HNE-, OxPC-, and OxCL-epitopes have been documented in atherosclerotic plaques of mice and humans (25,(31)(32)(33)(34)(35)(36).…”

Section: Low-density Lipoproteinmentioning

confidence: 99%

The OSE complotype and its clinical potential

Alic

Binder²,

Papac-Miličević³

2022

Front. Immunol.

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Cellular death, aging, and tissue damage trigger inflammation that leads to enzymatic and non-enzymatic lipid peroxidation of polyunsaturated fatty acids present on cellular membranes and lipoproteins. This results in the generation of highly reactive degradation products, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), that covalently modify free amino groups of proteins and lipids in their vicinity. These newly generated neoepitopes represent a unique set of damage-associated molecular patterns (DAMPs) associated with oxidative stress termed oxidation-specific epitopes (OSEs). OSEs are enriched on oxidized lipoproteins, microvesicles, and dying cells, and can trigger sterile inflammation. Therefore, prompt recognition and removal of OSEs is required to maintain the homeostatic balance. This is partially achieved by various humoral components of the innate immune system, such as natural IgM antibodies, pentraxins and complement components that not only bind OSEs but in some cases modulate their pro-inflammatory potential. Natural IgM antibodies are potent complement activators, and 30% of them recognize OSEs such as oxidized phosphocholine (OxPC-), 4-HNE-, and MDA-epitopes. Furthermore, OxPC-epitopes can bind the complement-activating pentraxin C-reactive protein, while MDA-epitopes are bound by C1q, C3a, complement factor H (CFH), and complement factor H-related proteins 1, 3, 5 (FHR-1, FHR-3, FHR-5). In addition, CFH and FHR-3 are recruited to 2-(ω-carboxyethyl)pyrrole (CEP), and full-length CFH also possesses the ability to attenuate 4-HNE-induced oxidative stress. Consequently, alterations in the innate humoral defense against OSEs predispose to the development of diseases associated with oxidative stress, as shown for the prototypical OSE, MDA-epitopes. In this mini-review, we focus on the mechanisms of the accumulation of OSEs, the pathophysiological consequences, and the interactions between different OSEs and complement components. Additionally, we will discuss the clinical potential of genetic variants in OSE-recognizing complement proteins – the OSE complotype - in the risk estimation of diseases associated with oxidative stress.

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Transfer and Enzyme-Mediated Metabolism of Oxidized Phosphatidylcholine and Lysophosphatidylcholine between Low- and High-Density Lipoproteins

Cited by 14 publications

References 34 publications

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

Targeting the Microenvironment of Vulnerable Atherosclerotic Plaques: An Emerging Diagnosis and Therapy Strategy for Atherosclerosis

The OSE complotype and its clinical potential

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