Erratum to: Modulation Peroxisome Proliferators Activated Receptor alpha (PPAR α) and Acyl Coenzyme A: Cholesterol Acyltransferase1 (ACAT1) Gene expression by Fatty Acids in Foam cell

Reza, Javad Zavvar; Doosti, Mahmood; Salehipour, Masoud; Packnejad, Malehieh; Mojarrad, Majed; Heidari, Mansour

doi:10.1186/1476-511x-8-47

Cited by 10 publications

(13 citation statements)

References 2 publications

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“…EPA and DHA are known to reduce foam cell accumulation in advanced human carotid plaques [25] and cholesteryl ester levels in THP-1 macrophages [26]. However, here we report that EPA elicits differential effects on the uptake of modified LDL as it reduces the uptake of AcLDL while promoting the uptake of OxLDL.…”

Section: Discussionmentioning

confidence: 70%

“…Nevertheless, increased expression of CD36 mRNA and protein levels could potentially explain the observed increase in OxLDL uptake in response to EPA. Interestingly, EPA has been shown to induce the expression of peroxisome proliferatoractivated receptors (PPAR)-a in THP-1 macrophages [26] and numerous studies have used PPAR agonists, such as thiazolidinedione, to delineate an anti-atherogenic role for these ligand-activated transcription factors during foam cell formation [42]. More specifically, it has now been shown that PPAR activation can induce the expression of CD36 [43,44], which in turn increases the amount of OxLDL internalized [45], while simultaneously promoting cholesterol efflux through the up-regulation of ATP-binding cassette transporter proteins A1 (ABCA-1) and G1 (ABCG-1) in human macrophages [46,47].…”

Section: Discussionmentioning

confidence: 99%

“…Some of the atheroprotective effects of n-3 PUFA in mice have been shown to involve changes in macrophage function [12,17] and a recent study found that EPA, delivered from n-3 PUFA ethyl esters, reduced foam cell accumulation in advanced human carotid plaques [25] suggesting that n-3 PUFA not only target macrophage activity but also foam cell formation. It has been found that EPA inhibits cholesteryl ester accumulation in THP-1 [26] and rat peritoneal macrophages [27] with the latter effect attributed to a reduction in acetylated LDL (AcLDL) receptor number. However, it has not been established whether EPA affects direct uptake of modified LDL in human macrophages and whether DHA, another key n-3 PUFA, is also able to regulate this process.…”

Section: Introductionmentioning

confidence: 99%

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Eicosapentaenoic Acid and Docosahexaenoic Acid Regulate Modified LDL Uptake and Macropinocytosis in Human Macrophages

McLaren

Michael

Guschina

et al. 2011

Lipids

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There is evidence that long chain n-3 PUFA (such as from fish oils) provide atheroprotection through, in part, changes in macrophage function although it has not been fully determined whether these n-3 PUFA target cellular mechanisms that control macrophage foam cell formation. Therefore, we investigated whether the n-3 PUFA, EPA and DHA, modulate modified low-density lipoprotein (LDL) uptake by human macrophages. The uptake of fluorophore labeled acetylated LDL (AcLDL) and/or oxidized LDL (OxLDL) by THP-1 macrophages and primary human monocyte-derived macrophages were measured by flow cytometry following co-incubation with EPA or DHA in vitro. DHA inhibited both AcLDL and OxLDL uptake in human macrophages whilst EPA reduced AcLDL and increased OxLDL uptake. These effects were only partly explained by changes in the mRNA and protein expression of key scavenger receptors, such as CD36 and scavenger receptor-A, in these cells suggesting the involvement of a scavenger receptor-independent mechanism. EPA and DHA inhibited macropinocytosis, as measured by Lucifer Yellow uptake, in human macrophages and attenuated the expression of Syndecan-4, which has been implicated in the uptake of other modified forms of LDL. EPA and DHA reduced modified LDL uptake by human macrophages through a mechanism that is in part scavenger receptor-independent and may involve inhibition of macropinocytosis and Syndecan-4 expression. This suggests that both EPA and DHA are capable of regulating macrophage foam cell formation and adds to the evidence describing an atheroprotective role for n-3 PUFA, implicating them as potential therapeutic agents for the treatment of clinical atherosclerosis.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Eicosapentaenoic Acid and Docosahexaenoic Acid Regulate Modified LDL Uptake and Macropinocytosis in Human Macrophages

McLaren

Michael

Guschina

et al. 2011

Lipids

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“…58,59 However, Campioli et al 33 showed a decrease in PPAR-γ transcript levels following MEHP treatment. In zebrafish hepatocytes, expression of PPAR subtypes was significantly induced by both DEHP and phthalic acid demonstrating that the PPAR subtype γ was less responsive to these treatments.…”

Section: ■ Experimental Proceduresmentioning

confidence: 96%

Effects of Diisodecyl Phthalate on PPAR:RXR-Dependent Gene Expression Pathways in Sea Bream Hepatocytes

Cocci

Mosconi

Arukwe

et al. 2015

Chem. Res. Toxicol.

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Evidence that endocrine-disrupting chemicals (EDCs) may target metabolic disturbances, beyond interference with the functions of the endocrine systems has recently accumulated. Among EDCs, phthalate plasticizers like the diisodecyl phthalate (DiDP) are commonly found contaminants of aquatic environments and have been suggested to function as obesogens by activating peroxisome proliferator activated receptors (PPARs), a subset of nuclear receptors (NRs) that act as metabolic sensors, playing pivotal roles in lipid homeostasis. However, little is known about the modulation of PPAR signaling pathways by DiDP in fish. In this study, we have first investigated the ligand binding efficiency of DiDP to the ligand binding domains of PPARs and retinoid-X-receptor-α (RXRα) proteins in fish using a molecular docking approach. Furthermore, in silico predictions were integrated by in vitro experiments to show possible dose-relationship effects of DiDP on PPAR:RXR-dependent gene expression pathways using sea bream hepatocytes. We observed that DiDP shows high binding efficiency with piscine PPARs demonstrating a greater preference for RXRα. Our studies also demonstrated the coordinate increased expression of PPARs and RXRα, as well as their downstream target genes in vitro. Principal component analysis (PCA) showed the strength of relationship between transcription of most genes involved in fatty acid metabolism and PPAR mRNA levels. In particular, fatty acid binding protein (FABP) was highly correlated to all PPARs. The results of this study suggest that DiDP can be considered an environmental stressor that activates PPAR:RXR signaling to promote long-term changes in lipid homeostasis leading to potential deleterious physiological consequences in teleost fish.

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“…These proteins also played pivotal roles in fatty acid synthesis and transport. ACAA1 is broadly expressed in humans and animals and can catalyze free cholesterol and long-chain fatty acids to synthesize esterified cholesterol [68]. ACAA1 is also a marker of beta-oxidation [69,70].…”

Section: Discussionmentioning

confidence: 99%

Short hairpin RNA attenuates liver fibrosis by regulating the peroxisome proliferator-activated receptor-γ and nuclear factor-κB pathways in hepatitis B virus-induced liver fibrosis in mice

Cao

Sun

et al. 2019

Preprint

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Background: Progressive liver fibrosis, caused by chronic viral infection and metabolic disorders, results in the development of cirrhosis and hepatocellular carcinoma. However, no antifibrotic therapies have been approved to date. In our previous study, adeno-associated virus (AAV) short hairpin RNAs (shRNAs) targeting hepatitis B virus (HBV) and transforming growth factor (TGF)-β administration could persistently inhibit HBV replication and concomitantly prevent liver fibrosis. However, the differentially expressed proteins and critical regulatory networks of AAVshRNA treatment remain unclear. Accordingly, in this study, our major goal was we aimed to analyze differentially expressed proteins in the liver of AAV-shRNAs-treated mice with HBV infection and liver fibrosis using isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomics and to elucidate the underlying antifibrotic mechanisms. Results: In total 2743 proteins were recognized by iTRAQ-based quantitative proteomics analysis. Gene ontology analysis suggested that the differentially expressed proteins were mostly participated in peptide metabolism in the biological process category, cytosolic ribosomes in the cell component category, and structural constituents of ribosomes in the molecular function category. Kyoto Encyclopedia of Genes and Genomespathway analysis indicated that oxidative stress and the peroxisome proliferator-activated receptor (PPAR) signaling pathway were actived after treatment. Verification studies showed that AAVshRNAs inhibited hepatic stellate cell activation and inflammation by suppressing nuclear factor-κB p65 phosphorylation and α-smooth muscle actin expression via upregulation of PPAR-γ. Hepatocytes steatosis was also decreased by activating PPAR signaling pathway and improving lipid metabolism. TGF-β level was decreased owning to increase PPAR-γ expression and directly inhibition using AAVshRNAs targeting TGF-β. TGF-β-induced oxidative stress was suppressed by increasing glutathione S-transferase Pi 1 and reducing peroxiredoxin 1. Conclusions: Our results indicated that AAV-shRNAs were effective for modulating liver fibrosis by reducing oxidative stress, inflammation and activating PPAR signaling pathway.

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Erratum to: Modulation Peroxisome Proliferators Activated Receptor alpha (PPAR α) and Acyl Coenzyme A: Cholesterol Acyltransferase1 (ACAT1) Gene expression by Fatty Acids in Foam cell

Cited by 10 publications

References 2 publications

Eicosapentaenoic Acid and Docosahexaenoic Acid Regulate Modified LDL Uptake and Macropinocytosis in Human Macrophages

Eicosapentaenoic Acid and Docosahexaenoic Acid Regulate Modified LDL Uptake and Macropinocytosis in Human Macrophages

Effects of Diisodecyl Phthalate on PPAR:RXR-Dependent Gene Expression Pathways in Sea Bream Hepatocytes

Short hairpin RNA attenuates liver fibrosis by regulating the peroxisome proliferator-activated receptor-γ and nuclear factor-κB pathways in hepatitis B virus-induced liver fibrosis in mice

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