Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein

Namgaladze, Dmitry; Jennewein, Carla; Preiß, Stefan; Knethen, Andreas von; Brüne, Bernhard

doi:10.1194/jlr.m800615-jlr200

Cited by 5 publications

(4 citation statements)

References 37 publications

(62 reference statements)

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“…In atherosclerosis, ongoing inflammation and accumulation of apoptotic/necrotic material are observed, suggesting defects of phagocytes in recognizing or responding to dying cells. Both apoptosis and necrosis were observed after oxLDL treatment in THP-1 monocytes and Jurkat T-lymphoma cells [99] (Fig. 1).…”

Section: Discussionmentioning

confidence: 92%

“…1). In particular, preincubating RAW 264.7 or human macrophages with apoptotic cells decreased PMAstimulated superoxide generation, but oxLDL apparently suppressed changes in apoptotic cells that interfered with superoxide and inflammatory cytokines generation in phagocytes, suggesting that oxLDL induced cell death may contribute to a proinflammatory microenvironment in the atherosclerotic plaque [99].…”

Section: Discussionmentioning

confidence: 94%

“…1). Macrophages ingesting apoptotic cells attenuate inflammatory responses, such as ROS generation and TNF-and IL-6 production [99]. Modified lipoproteins such as oxLDL are known to promote inflammation and t interfere with apoptotic cell clearance (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Peluso

Morabito²,

Urban³

et al. 2012

EMIDDT

197

133

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The involvement of both oxidative stress and hyperlipaemia in atherosclerosis development is well established. Oxidative burst is an innate immune response to infection, the latter being associated also with marked changes in lipid and lipoprotein metabolism, aimed to neutralize endotoxin toxic effects. On the other hand, lipid overload may increase lipopolysaccharide circulating levels and oxidative stress. Whilst these changes may be beneficial from the perspective of host defense, if they become chronic, they likely increase the risk of atherosclerosis. In particular, oxidation of lipoproteins, resulting from an imbalance of the pro- and antioxidant equilibrium, is involved in the pathologic process of atherosclerosis, changing cellular functions. Lipid oxidation, induced by leukocytes derived reactive oxygen species, can amplify foam cell formation through oxidized low density lipoproteins LDL (oxLDL) formation and uptake. The main enzymes, operating during oxidative burst, involved in LDL oxidation are NADPH oxidase and myeloperoxidase. In vitro studies have shown that oxLDL are able to induce many proatherogenic processes, including modulation of oxidative burst. OxLDL may also induce maturation of dendritic cells and regulate the shift from classical (M1) to alternative (M2) macrophage activation and from T helper 1 to T helper 2 response, suggesting that these could act as a bridge between innate and adaptative immunity, both involved in plaque development. Understanding the relationship between oxLDL and leukocyte oxidative burst helps to explain the involvement of innate immune responses in the early phases of atherosclerosis. The present review focuses on this interplay.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 94%

See 1 more Smart Citation

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Peluso

Morabito²,

Urban³

et al. 2012

EMIDDT

197

133

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“…Thus the prior history of an apoptotic cell, including microbe infection, previous ligation of TLRs, cholesterol loading, an encounter with cholesterol crystals, or in one study, prior exposure to oxLDL (1280), can modulate the effect of its subsequent phagocytosis by another cell from anti-inflammatory to proinflammatory (1431,2120). Indeed, one can imagine that the complex array of proinflammatory triggers encountered deep within an actively growing atherosclerotic plaque could lead to repeated cycles of apoptosis and necrosis followed by toxic or proinflammatory efferocytosis, converting the necrotic core into an immunological "no-man's land.…”

Section: Macrophage-dependent Resolution Of Inflammation: An Optimal mentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

384

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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FABP4 inhibition suppresses PPARγ activity and VLDL-induced foam cell formation in IL-4-polarized human macrophages

et al. 2015

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Attenuated suppression of the oxidative burst by cells dying in the presence of oxidized low density lipoprotein

Cited by 5 publications

References 37 publications

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

Molecular Biology of Atherosclerosis

FABP4 inhibition suppresses PPARγ activity and VLDL-induced foam cell formation in IL-4-polarized human macrophages

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