L5-LDL from ST-elevation myocardial infarction patients induces IL-1β production via LOX-1 and NLRP3 inflammasome activation in macrophages

Yang, Tsung-Chieh; Chang, Po‐Yuan; Lu, Shao‐Chun

doi:10.1152/ajpheart.00509.2016

Cited by 51 publications

(37 citation statements)

References 50 publications

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“…This occurred in the absence of changes in cell proliferation or mortality. According to our results, in THP1 macrophages, L5 from infarcted patients also induced IL1β release [17], and L5 from rabbits fed an atherogenic diet induced IL1β and IL6 [19]. The induction of IL10, a cytokine that suppresses macrophage activation and inflammation [35], could regulate an excessive inflammatory response to LDL(−), as was previously described in circulating monocytes [31].…”

Section: Discussionsupporting

confidence: 80%

“…Their expression increases in differentiated macrophages vs. monocytes, as they are highly expressed in lipid-laden macrophages, and particularly in the presence of stimuli, such as OxLDL [42,43]. Previous studies have reported the involvement of these receptors in some LDL(−) actions in macrophages [16,17]. Taken together, these observations suggest the involvement of LOX-1 and CD36 in the LDL(−) effects described in the current study.…”

Section: Discussionsupporting

confidence: 78%

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Electronegative LDL Promotes Inflammation and Triglyceride Accumulation in Macrophages

Puig

Montolio²,

Camps‐Renom

et al. 2020

Cells

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Electronegative low-density lipoprotein (LDL) (LDL(−)), a modified LDL that is present in blood and exerts atherogenic effects on endothelial cells and monocytes. This study aimed to determine the action of LDL(−) on monocytes differentiated into macrophages. LDL(−) and in vitro-modified LDLs (oxidized, aggregated, and acetylated) were added to macrophages derived from THP1 monocytes over-expressing CD14 (THP1-CD14). Then, cytokine release, cell differentiation, lipid accumulation, and gene expression were measured by ELISA, flow cytometry, thin-layer chromatography, and real-time PCR, respectively. LDL(−) induced more cytokine release in THP1-CD14 macrophages than other modified LDLs. LDL(−) also promoted morphological changes ascribed to differentiated macrophages. The addition of high-density lipoprotein (HDL) and anti-TLR4 counteracted these effects. LDL(−) was highly internalized by macrophages, and it was the major inductor of intracellular lipid accumulation in triglyceride-enriched lipid droplets. In contrast to inflammation, the addition of anti-TLR4 had no effect on lipid accumulation, thus suggesting an uptake pathway alternative to TLR4. In this regard, LDL(−) upregulated the expression of the scavenger receptors CD36 and LOX-1, as well as several genes involved in triglyceride (TG) accumulation. The importance and novelty of the current study is that LDL(−), a physiologically modified LDL, exerted atherogenic effects in macrophages by promoting differentiation, inflammation, and triglyceride-enriched lipid droplets formation in THP1-CD14 macrophages, probably through different receptors.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 78%

Electronegative LDL Promotes Inflammation and Triglyceride Accumulation in Macrophages

Puig

Montolio²,

Camps‐Renom

et al. 2020

Cells

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show abstract

“…Modified LDLs play a key role in atherogenesis and atherosclerosis progression, and induce atherosclerotic lesions through complex inflammatory and immunological mechanisms [ 19 ]. In the vascular wall, modified lipoproteins act as toxic compounds, thereby promoting foam cell activation, macrophage proliferation and migration, as well as excessive matrix extracellular remodeling by increased metalloproteinase (MMP) production [ 46 , 47 , 48 , 49 ]. The presence of modified LDLs in the vascular wall, together with pro-inflammatory cytokines, high levels of nitric oxide, and mechanical injury, can lead to apoptosis of VSMCs, which produces fibrous cap thinning and necrotic core formation, with calcification of the atherosclerotic plaques [ 50 ].…”

Section: Lrp1 In the Metabolic Syndromementioning

confidence: 99%

The Role of Low-Density Lipoprotein Receptor-Related Protein 1 in Lipid Metabolism, Glucose Homeostasis and Inflammation

Dato

Chiabrando

2018

IJMS

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Metabolic syndrome (MetS) is a highly prevalent disorder which can be used to identify individuals with a higher risk for cardiovascular disease and type 2 diabetes. This metabolic syndrome is characterized by a combination of physiological, metabolic, and molecular alterations such as insulin resistance, dyslipidemia, and central obesity. The low-density lipoprotein receptor-related protein 1 (LRP1—A member of the LDL receptor family) is an endocytic and signaling receptor that is expressed in several tissues. It is involved in the clearance of chylomicron remnants from circulation, and has been demonstrated to play a key role in the lipid metabolism at the hepatic level. Recent studies have shown that LRP1 is involved in insulin receptor (IR) trafficking and intracellular signaling activity, which have an impact on the regulation of glucose homeostasis in adipocytes, muscle cells, and brain. In addition, LRP1 has the potential to inhibit or sustain inflammation in macrophages, depending on its cellular expression, as well as the presence of particular types of ligands in the extracellular microenvironment. In this review, we summarize existing perspectives and the latest innovations concerning the role of tissue-specific LRP1 in lipoprotein and glucose metabolism, and examine its ability to mediate inflammatory processes related to MetS and atherosclerosis.

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“…The search did not include the use of antibodies for flow cytometry, ELISAs, or blocking studies. From the search results, we evaluated all articles published in 2017, for a total of 28 articles ( 2 , 8 – 11 , 13 , 15 , 16 , 19 , 21 , 22 , 26 – 28 , 30 , 32 , 34 , 41 , 42 , 44 , 45 , 47 , 48 , 50 – 52 , 54 , 58 ). Of these, 79% (22 of 28 articles) used immunoblot analysis, and 39% (11 of 28 articles) used immunohistochemistry (5 articles of the 28 evaluated used both techniques, 18%).…”

Section: Antibody Use In American Journal Of Physiology-heamentioning

confidence: 99%

Guidelines for authors and reviewers on antibody use in physiology studies

Brooks

Lindsey

2018

American Journal of Physiology-Heart and Circulatory Physiology

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Antibody use is a critical component of cardiovascular physiology research, and antibodies are used to monitor protein abundance (immunoblot analysis) and protein expression and localization (in tissue by immunohistochemistry and in cells by immunocytochemistry). With ongoing discussions on how to improve reproducibility and rigor, the goal of this review is to provide best practice guidelines regarding how to optimize antibody use for increased rigor and reproducibility in both immunoblot analysis and immunohistochemistry approaches.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/guidelines-on-antibody-use-in-physiology-studies/.

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L5-LDL from ST-elevation myocardial infarction patients induces IL-1β production via LOX-1 and NLRP3 inflammasome activation in macrophages

Cited by 51 publications

References 50 publications

Electronegative LDL Promotes Inflammation and Triglyceride Accumulation in Macrophages

Electronegative LDL Promotes Inflammation and Triglyceride Accumulation in Macrophages

The Role of Low-Density Lipoprotein Receptor-Related Protein 1 in Lipid Metabolism, Glucose Homeostasis and Inflammation

Guidelines for authors and reviewers on antibody use in physiology studies

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