The anti-inflammatory effect of paraoxonase 1 against oxidized lipids depends on its association with high density lipoproteins

Loued, Soumaya; Isabelle, Maxim; Berrougui, Hicham; Khalil, Abdelouahed

doi:10.1016/j.lfs.2011.10.018

Cited by 30 publications

(34 citation statements)

References 35 publications

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“…In vitro studies have demonstrated that purified PON1 had an anti-inflammatory effect in the presence of HDL, causing a 3-fold reduction in ICAM-1 levels. PON1 also significantly decreased TNF␣ and oxidized phospholipid induced ICAM-1 expression (22). This indicates PON1 associated with HDL is required for its antioxidant and anti-inflammatory functions.…”

mentioning

confidence: 79%

Impairment of High-Density Lipoprotein Resistance to Lipid Peroxidation and Adipose Tissue Inflammation in Obesity Complicated by Obstructive Sleep Apnea

Yadav

Aghamohammadzadeh

Liu

et al. 2014

The Journal of Clinical Endocrinology &Amp; Metabolism

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mentioning

confidence: 79%

Impairment of High-Density Lipoprotein Resistance to Lipid Peroxidation and Adipose Tissue Inflammation in Obesity Complicated by Obstructive Sleep Apnea

Yadav

Aghamohammadzadeh

Liu

et al. 2014

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…Briefly, and described by Loued et al [23], competent Origami BÒ cells were transformed with the pET32b plasmid (G3C9-8His) encoding the PON1 sequence and a histidine tag. The cells were grown in 2xTY medium for 8 h at 30°C then for 12 h at 20°C.…”

Section: Expression and Purification Of Human Recombinant Pon1 (Hrpon1)mentioning

confidence: 99%

Paraoxonase 1‐treated oxLDL promotes cholesterol efflux from macrophages by stimulating the PPARγ–LXRα–ABCA1 pathway

et al. 2016

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Edited by Laszlo NagyHere, we investigate the mechanism through which paraoxonase 1 (PON1) may regulate cholesterol efflux. Pretreatment of oxLDL with PON1 (oxLDL-PON1) contributed to the formation of LysoPC. In J774 macrophages, oxLDL-PON1 increased cholesterol efflux by more than 47% compared to oxLDL alone. oxLDL-PON1 significantly increased mRNA and protein expression of ABCA1 and ABCG1, as well as of PPARc and LXRa compared to oxLDL alone. Intraperitoneal injection of oxLDL-PON1-or LysoPC-treated J774 macrophages significantly increased the fecal elimination of macrophage-derived cholesterol in these mice. Our results suggest that PON1 stimulates cholesterol efflux via a mechanism that involves oxidized phospholipid hydrolysis.

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“…Previous studies have shown that in vitro enrichment of HDL with human PON1 improves the functionality of HDL by, in part, increasing their anti-inflammatory activity as well as their capacity to mediate macrophage-derived cholesterol efflux [8,10]. In the present study, we investigated the effect of the overexpression of human PON1 in mice on the capacity of HDL to mediate cholesterol homeostasis in vitro and in vivo and to elucidate the mechanism of this regulation.…”

Section: Resultsmentioning

confidence: 96%

“…While the physiologic role of PON1 is not clear, it has been suggested that it hydrolyzes oxidized phospholipids in oxLDL, abolishing their biological activities [10]. Loued et al recently showed that PON1 possesses phospholipase-A2-like activity that allows it to hydrolyze oxidized phospholipids at the sn- 2 position, contributing to the formation of lysophosphatidylcholine [10]. …”

Section: Introductionmentioning

confidence: 99%

Human paraoxonase 1 overexpression in mice stimulates HDL cholesterol efflux and reverse cholesterol transport

Ikhlef¹,

Berrougui

Simo³

et al. 2017

PLoS ONE

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This study was aimed to investigate the effect of human PON1 overexpression in mice on cholesterol efflux and reverse cholesterol transport. PON1 overexpression in PON1-Tg mice induced a significant 3-fold (p<0.0001) increase in plasma paraoxonase activity and a significant ~30% (p<0.0001) increase in the capacity of HDL to mediate cholesterol efflux from J774 macrophages compared to wild-type mice. It also caused a significant 4-fold increase (p<0.0001) in the capacity of macrophages to transfer cholesterol to apoA-1, a significant 2-fold (p<0.0003) increase in ABCA1 mRNA and protein expression, and a significant increase in the expression of PPARγ (p<0.0003 and p<0.04, respectively) and LXRα (p<0.0001 and p<0.01, respectively) mRNA and protein compared to macrophages from wild-type mice. Moreover, transfection of J774 macrophages with human PON1 also increased ABCA1, PPARγ and LXRα protein expression and stimulates macrophages cholesterol efflux to apo A1. In vivo measurements showed that the overexpression of PON1 significantly increases the fecal elimination of macrophage-derived cholesterol in PON1-Tg mice. Overall, our results suggested that the overexpression of PON1 in mice may contribute to the regulation of the cholesterol homeostasis by improving the capacity of HDL to mediate cholesterol efflux and by stimulating reverse cholesterol transport.

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The anti-inflammatory effect of paraoxonase 1 against oxidized lipids depends on its association with high density lipoproteins

Cited by 30 publications

References 35 publications

Impairment of High-Density Lipoprotein Resistance to Lipid Peroxidation and Adipose Tissue Inflammation in Obesity Complicated by Obstructive Sleep Apnea

Impairment of High-Density Lipoprotein Resistance to Lipid Peroxidation and Adipose Tissue Inflammation in Obesity Complicated by Obstructive Sleep Apnea

Paraoxonase 1‐treated oxLDL promotes cholesterol efflux from macrophages by stimulating the PPARγ–LXRα–ABCA1 pathway

Human paraoxonase 1 overexpression in mice stimulates HDL cholesterol efflux and reverse cholesterol transport

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