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Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling

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Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling. / Cappello, Christian; Saugel, Bernd; Huth, Karin C; Zwergal, Andreas; Krautkrämer, Martina; Furman, Christophe; Rouis, Mustapha; Wieser, Bianca; Schneider, Heike W; Neumeier, Dieter; Brand, Korbinian.

In: ARTERIOSCL THROM VAS, Vol. 27, No. 1, 01.01.2007, p. 226-32.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Cappello, C, Saugel, B, Huth, KC, Zwergal, A, Krautkrämer, M, Furman, C, Rouis, M, Wieser, B, Schneider, HW, Neumeier, D & Brand, K 2007, 'Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling', ARTERIOSCL THROM VAS, vol. 27, no. 1, pp. 226-32. https://doi.org/10.1161/01.ATV.0000250615.27795.85

APA

Cappello, C., Saugel, B., Huth, K. C., Zwergal, A., Krautkrämer, M., Furman, C., Rouis, M., Wieser, B., Schneider, H. W., Neumeier, D., & Brand, K. (2007). Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling. ARTERIOSCL THROM VAS, 27(1), 226-32. https://doi.org/10.1161/01.ATV.0000250615.27795.85

Vancouver

Cappello C, Saugel B, Huth KC, Zwergal A, Krautkrämer M, Furman C et al. Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling. ARTERIOSCL THROM VAS. 2007 Jan 1;27(1):226-32. https://doi.org/10.1161/01.ATV.0000250615.27795.85

Bibtex

@article{90600b2712f648d58c880ef8515b9ff5,
title = "Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling",
abstract = "OBJECTIVE: Recent studies have provided strong evidence for the presence of ozone in atherosclerotic lesions. In addition, modification of LDL has been suggested to be involved in atherosclerosis. In the present study we wanted to investigate whether LDL exposed to ozone (ozLDL) is able to modulate the NF-kappaB system, as a paradigm for inflammatory signaling.METHODS AND RESULTS: We showed that activation of NF-kappaB by lipopolysaccharide (LPS), a prototypic inducer of innate immunity, was reversibly inhibited by ozLDL in monocytic THP-1 cells in a dose-dependent manner, whereas tumor necrosis factor (TNF) signaling was not affected. This was not attributable to a direct ozone effect or solely the presence of lipoprotein, and neither required direct contact to LPS nor was accompanied by a change in LPS binding. Comparable inhibitory effects of ozLDL were observed in human monocyte/macrophages and endothelial cells. The presence of ozLDL led to a decrease in LPS-induced IkappaB alpha proteolysis and a reduction of kappaB-dependent transcription/target-gene expression. Furthermore, ozLDL markedly lowered stimulus-induced IkappaB kinase (IKK) activity and phosphorylation/proteolysis of interleukin (IL)-1 receptor-associated kinase-1 (IRAK-1). Finally, cholesterol ozonization products were identified as effective ozLDL inhibitory compounds.CONCLUSIONS: Our study demonstrated that ozLDL inhibited NF-kappaB and IRAK-1-associated signaling which may impair immune function and promote apoptosis.",
keywords = "Apoptosis, Atherosclerosis, Cell Line, Dose-Response Relationship, Drug, Endothelium, Vascular, Enzyme Activation, Humans, Interleukin-1 Receptor-Associated Kinases, Lipopolysaccharides, Lipoproteins, LDL, Monocytes, NF-kappa B, Ozone, Phosphorylation, Signal Transduction",
author = "Christian Cappello and Bernd Saugel and Huth, {Karin C} and Andreas Zwergal and Martina Krautkr{\"a}mer and Christophe Furman and Mustapha Rouis and Bianca Wieser and Schneider, {Heike W} and Dieter Neumeier and Korbinian Brand",
year = "2007",
month = jan,
day = "1",
doi = "10.1161/01.ATV.0000250615.27795.85",
language = "English",
volume = "27",
pages = "226--32",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

RIS

TY - JOUR

T1 - Ozonized low density lipoprotein (ozLDL) inhibits NF-kappaB and IRAK-1-associated signaling

AU - Cappello, Christian

AU - Saugel, Bernd

AU - Huth, Karin C

AU - Zwergal, Andreas

AU - Krautkrämer, Martina

AU - Furman, Christophe

AU - Rouis, Mustapha

AU - Wieser, Bianca

AU - Schneider, Heike W

AU - Neumeier, Dieter

AU - Brand, Korbinian

PY - 2007/1/1

Y1 - 2007/1/1

N2 - OBJECTIVE: Recent studies have provided strong evidence for the presence of ozone in atherosclerotic lesions. In addition, modification of LDL has been suggested to be involved in atherosclerosis. In the present study we wanted to investigate whether LDL exposed to ozone (ozLDL) is able to modulate the NF-kappaB system, as a paradigm for inflammatory signaling.METHODS AND RESULTS: We showed that activation of NF-kappaB by lipopolysaccharide (LPS), a prototypic inducer of innate immunity, was reversibly inhibited by ozLDL in monocytic THP-1 cells in a dose-dependent manner, whereas tumor necrosis factor (TNF) signaling was not affected. This was not attributable to a direct ozone effect or solely the presence of lipoprotein, and neither required direct contact to LPS nor was accompanied by a change in LPS binding. Comparable inhibitory effects of ozLDL were observed in human monocyte/macrophages and endothelial cells. The presence of ozLDL led to a decrease in LPS-induced IkappaB alpha proteolysis and a reduction of kappaB-dependent transcription/target-gene expression. Furthermore, ozLDL markedly lowered stimulus-induced IkappaB kinase (IKK) activity and phosphorylation/proteolysis of interleukin (IL)-1 receptor-associated kinase-1 (IRAK-1). Finally, cholesterol ozonization products were identified as effective ozLDL inhibitory compounds.CONCLUSIONS: Our study demonstrated that ozLDL inhibited NF-kappaB and IRAK-1-associated signaling which may impair immune function and promote apoptosis.

AB - OBJECTIVE: Recent studies have provided strong evidence for the presence of ozone in atherosclerotic lesions. In addition, modification of LDL has been suggested to be involved in atherosclerosis. In the present study we wanted to investigate whether LDL exposed to ozone (ozLDL) is able to modulate the NF-kappaB system, as a paradigm for inflammatory signaling.METHODS AND RESULTS: We showed that activation of NF-kappaB by lipopolysaccharide (LPS), a prototypic inducer of innate immunity, was reversibly inhibited by ozLDL in monocytic THP-1 cells in a dose-dependent manner, whereas tumor necrosis factor (TNF) signaling was not affected. This was not attributable to a direct ozone effect or solely the presence of lipoprotein, and neither required direct contact to LPS nor was accompanied by a change in LPS binding. Comparable inhibitory effects of ozLDL were observed in human monocyte/macrophages and endothelial cells. The presence of ozLDL led to a decrease in LPS-induced IkappaB alpha proteolysis and a reduction of kappaB-dependent transcription/target-gene expression. Furthermore, ozLDL markedly lowered stimulus-induced IkappaB kinase (IKK) activity and phosphorylation/proteolysis of interleukin (IL)-1 receptor-associated kinase-1 (IRAK-1). Finally, cholesterol ozonization products were identified as effective ozLDL inhibitory compounds.CONCLUSIONS: Our study demonstrated that ozLDL inhibited NF-kappaB and IRAK-1-associated signaling which may impair immune function and promote apoptosis.

KW - Apoptosis

KW - Atherosclerosis

KW - Cell Line

KW - Dose-Response Relationship, Drug

KW - Endothelium, Vascular

KW - Enzyme Activation

KW - Humans

KW - Interleukin-1 Receptor-Associated Kinases

KW - Lipopolysaccharides

KW - Lipoproteins, LDL

KW - Monocytes

KW - NF-kappa B

KW - Ozone

KW - Phosphorylation

KW - Signal Transduction

U2 - 10.1161/01.ATV.0000250615.27795.85

DO - 10.1161/01.ATV.0000250615.27795.85

M3 - SCORING: Journal article

C2 - 17053167

VL - 27

SP - 226

EP - 232

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 1

ER -