<scp>CD</scp>36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate

Lu, Zhongyang; Li, Yanchun; Brinson, Colleen W.; Kirkwood, Keith L.; Lopes‐Virella, Maria F.; Huang, Yan

doi:10.1111/odi.12596

Cited by 19 publications

(23 citation statements)

References 49 publications

(68 reference statements)

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“…This may indicate the indirect PA activation of TLR4, by increasing the production of some noncanonical TLR4 activators. The explanation may also be that PA enhances the signal transduction, or that TLR4 forms complexes with other receptors, e.g., with cluster of differentiation 36 (CD36), through which TLR4 may be activated by PA [103]. Nevertheless, it is possible that PA may directly activate TLR4, as well as indirectly by inducing the same signaling pathways causing ER stress and generation of DAGs and ceramides in the cell.…”

Section: Palmitic Acid Is a Toll-like Receptor Agonistmentioning

confidence: 99%

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The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms

2019

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Palmitic acid is a saturated fatty acid whose blood concentration is elevated in obese patients. This causes inflammatory responses, where toll-like receptors (TLR), TLR2 and TLR4, play an important role. Nevertheless, palmitic acid is not only a TLR agonist. In the cell, this fatty acid is converted into phospholipids, diacylglycerol and ceramides. They trigger the activation of various signaling pathways that are common for LPS-mediated TLR4 activation. In particular, metabolic products of palmitic acid affect the activation of various PKCs, ER stress and cause an increase in ROS generation. Thanks to this, palmitic acid also strengthens the TLR4-induced signaling. In this review, we discuss the mechanisms of inflammatory response induced by palmitic acid. In particular, we focus on describing its effect on ER stress and IRE1α, and the mechanisms of NF-κB activation. We also present the mechanisms of inflammasome NLRP3 activation and the effect of palmitic acid on enhanced inflammatory response by increasing the expression of FABP4/aP2. Finally, we focus on the consequences of inflammatory responses, in particular, the effect of TNF-α, IL-1β and IL-6 on insulin resistance. Due to the high importance of macrophages and the production of proinflammatory cytokines by them, this work mainly focuses on these cells.

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Section: Palmitic Acid Is a Toll-like Receptor Agonistmentioning

confidence: 99%

“…Inhibition of PPARγ enhances the activity of IKK and NF-κB [170] and reduces the expression of CD36 [170, 172]. However, it should be noted that PA increases the expression of CD36 by inducing the ER stress [43, 83, 103, 173].…”

Section: Fatty Acid-binding Protein 4/ap2 and Peroxisome Proliferatormentioning

confidence: 99%

The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms

2019

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“…As a result of its expression in multiple cell types, it can be involved in a variety of biological processes, including transport of oxidized LDL (oxLDL) and fatty acids by macrophages and monocytes, and it participates in processes of inflammation, phagocytosis, and endocytosis [ 12 , 13 ]. In addition, a wide variety of studies have investigated the important roles CD36 plays in many disorders, such as coronary heart disease, hypertension, Alzheimer's Disease, insulin resistance, and metabolic syndrome [ 14 – 17 ]. However, the relationship between CD36 gene polymorphisms and the risk of ICH has not yet been studied.…”

Section: Introductionmentioning

confidence: 99%

CD36 Gene Polymorphisms Are Associated with Intracerebral Hemorrhage Susceptibility in a Han Chinese Population

Gong

Liao

Liu

et al. 2017

BioMed Research International

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The CD36 gene encodes a membrane glycoprotein (type B scavenger receptor, SR-B2) that plays a crucial role in lipid sensing, innate immunity, atherogenesis, and glycolipid metabolism. In this study, we aimed to investigate the association between CD36 gene polymorphisms and intracerebral hemorrhage (ICH) in a Han Chinese population. We performed genotype and allele analyses for eleven single nucleotide polymorphisms (SNPs) of CD36 in a case-controlled study involving 292 ICH patients and 298 control participants. Eleven SNPs were genotyped by the Improved Multiple Ligase Detection Reaction (iMLDR) method. The results indicated that the SNP rs1194182 values were significantly different between ICH group and control group in a dominant model after adjusting for confounding factors. The subgroup analysis conducted for rs1194182 showed that the allele G frequencies were significantly different between ICH patients and controls in hypertension group via a dominant model. We then analyzed the rs1194182 genotype distributions among different groups of the serum lipid groups, including BMI, TC, TG, HDL, and LDL. However, no significant differences were found in the analysis of other subgroups. Taken together, these findings indicate that rs1194182 polymorphism in the CD36 gene was associated with ICH, and genotype GG could be an independent predictor.

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“…Interestingly, CD36 was also implicated in the progression of periodontitis in mice (Lu et al . 2017) and humans (Li et al . 2019) with metabolic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Blockade of fatty acid signalling inhibits lipopolysaccharide‐induced macrophage recruitment and progression of apical periodontitis

et al. 2021

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Aim To examine the role of palmitic acid in lipopolysaccharide (LPS)‐stimulated chemotaxis of macrophages and the potential contribution of saturated fatty acid in signalling during the pathogenesis of apical periodontitis. Methodology J774, a mouse macrophage cell line, was used in the experiments. After treatment with LPS, proteolytic maturation of sterol regulatory element‐binding protein‐1c (SREBP‐1c) and expression of fatty acid synthase (FASN) were examined by Western analysis. Levels of palmitic acid were measured by reverse phase‐high performance liquid chromatography‐mass spectrometry. Knockdown of SREBP‐1c and FASN was accomplished by small interfering RNA technology. Secretion of CC‐chemokine ligand 2 (CCL2) and cellular chemotaxis were assessed by enzyme‐linked immunosorbent assay and transwell migration assay, respectively. Sulfo‐N‐succinimidyl oleate (SSO) treatment was used to inhibit fatty acid signalling in vitro and also in a rat model of apical periodontitis. All data were first subjected to Levene’s test. In vitro data were then analysed using ANOVA followed by Tukey’s multiple comparison test. Data from animal experiments were analysed by independent t‐tests. The significant level was set at 0.05. Results LPS stimulated proteolytic maturation of SREBP‐1c and FASN expression in macrophages and significantly enhanced palmitic acid synthesis (P < 0.05). Knockdown of SREBP‐1c attenuated LPS‐enhanced FASN expression. Knockdown of FASN significantly suppressed LPS‐enhanced palmitic acid synthesis (P < 0.05). LPS and exogenous palmitic acid significantly enhanced CCL2 secretion and macrophage chemotaxis (all P < 0.05). Inhibition of FASN expression significantly alleviated LPS‐augmented CCL2 secretion (P < 0.05). SSO significantly suppressed CCL2 secretion and macrophage chemotaxis augmented by LPS and palmitic acid (all P < 0.05). In a rat model of induced apical periodontitis, SSO treatment significantly attenuated progression of apical periodontitis and macrophage recruitment (all P < 0.05). Conclusions LPS/SREBP‐1c/FASN/palmitic acid signalling contributed to tissue destruction caused by bacterial infection. Modulation of lipid metabolism and signalling may be helpful for the management of apical periodontitis.

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CD36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate

Abstract: BACKGROUND-We reported that high-fat diet (HFD)-induced metabolic syndrome (MetS) exacerbates lipopolysaccharide (LPS)-stimulated periodontitis and palmitate, the major saturated fatty acid in the HFD, amplified LPS-stimulated gene expression in vitro. Since CD36 is a major

Cited by 19 publications

References 49 publications

The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms

The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms

CD36 Gene Polymorphisms Are Associated with Intracerebral Hemorrhage Susceptibility in a Han Chinese Population

Blockade of fatty acid signalling inhibits lipopolysaccharide‐induced macrophage recruitment and progression of apical periodontitis

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