A link between diabetes and atherosclerosis: Glucose regulates expression of CD36 at the level of translation

Griffin, E.L.; Re, Alessandro; Hamel, Nance; Fu, Chenzong; Bush, Harry L.; McCaffrey, Timothy A.; Asch, Adam S.

doi:10.1038/89969

Cited by 227 publications

(201 citation statements)

References 43 publications

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“…CD36 can be up-regulated by different molecules, in particular by high glucose concentrations [30], oxidatively modified LDL [31] and two oxidized linoleic acid metabolites, 9-hydroxyoctadecadienoic acid (9-HODE) and 13-HODE [13]. IL-4, a Th2 cytokine, has been shown to increase monocyte/Mu expression of CD36 [17], whereas expression of CD36 is down-regulated in response to a Th1 cytokine like IFN-c [32] and to LPS or dexamethasone [17].…”

Section: Discussionmentioning

confidence: 99%

IL‐13 induces expression of CD36 in human monocytes through PPARγ activation

et al. 2007

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The class B scavenger receptor CD36 is a component of the pattern recognition receptors on monocytes that recognizes a variety of molecules. CD36 expression in monocytes depends on exposure to soluble mediators. We demonstrate here that CD36 expression is induced in human monocytes following exposure to IL-13, a Th2 cytokine, via the peroxisome proliferator-activated receptor (PPAR)c pathway. Induction of CD36 protein was paralleled by an increase in CD36 mRNA. The PPARc pathway was demonstrated using transfection of a PPARc expression plasmid into the murine macrophage cell line RAW264.7, expressing very low levels of PPARc, and in peritoneal macrophages from PPARc-conditional null mice. We also show that CD36 induction by IL-13 via PPARc is dependent on phospholipase A2 activation and that IL-13 induces the production of endogenous 15-deoxy-D 12,14 -prostaglandin J 2 , an endogenous PPARc ligand, and its nuclear localization in human monocytes. Finally, we demonstrate that CD36 and PPARc are involved in IL-13-mediated phagocytosis of Plasmodium falciparum-parasitized erythrocytes. These results reveal a novel role for PPARc in the alternative activation of monocytes by IL-13, suggesting that endogenous PPARc ligands, produced by phospholipase A2 activation, could contribute to the biochemical and cellular functions of CD36.Leukocyte signaling * These 2 authors contributed equally to this work. IntroductionThe innate immune system protects the host in the early phase of infection. Circulating monocytes and tissue macrophages (Mu) mediate much of this innate immune response [1]. The strategy of recognition in the innate response is mediated by the coordinated action of pathogen-associated molecular patterns and pattern recognition receptors. Scavenger receptors and mannose receptor are important pattern recognition receptors in monocytes/Mu [2,3]. The modulation of the expression of these receptors may be critical in the role of these cells in antigen processing, scavenging, and host defence against pathogens. Several members of the scavenger receptor family, including Mu class A scavenger receptors and CD36, have been identified as receptors for modified lipoproteins on Mu, and their relevance to lipid uptake has been demonstrated in vitro and in vivo [4]. The scavenger receptor CD36, an 88-kDa integral membrane protein, is a class B scavenger receptor expressed on a wide variety of cells, in particular on monocytes and monocytederived Mu [5,6]. CD36 is known as a receptor for the uptake of oxidatively modified low-density lipoprotein (LDL) [7] and is also able to bind anionic phospholipid phosphatidylserine [8]. This scavenger receptor is implicated in the clearance of apoptotic cells [9]. Recently, McGilvray and colleagues [10] described a CD36-dependent nonopsonic phagocytosis of erythrocytes containing P. falciparum, by monocytes and culture-derived Mu, and a decrease in the parasiteinduced TNF secretion by monocytes/Mu. These processes were accentuated by CD36 up-regulation by peroxisome proliferator-acti...

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Section: Discussionmentioning

confidence: 99%

IL‐13 induces expression of CD36 in human monocytes through PPARγ activation

et al. 2007

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“…Thiazolidinediones, a major new class of drugs to treat diabetes, up regulate CD36 in monocytes/macrophages, adipose and muscle (Wilmsen, Ciaraldi, Carter, Reehman, Mudaliar, & Henry, 2003, Kolak, et al, 2006, Hirakata, Tozawa, Imura, & Sugiyama, 2004,Llaverias, et al, 2006, and may therefore contribute to the insulin-sensitizing effects of these drugs as a result of plasma fatty acid clearance, but also potentially to atherosclerosis and obesity in these patients. Interestingly, glucose/insulin appears to increase CD36 expression (Sampson, Davies, Braschi, Ivory, & Hughes, 2003,Griffin, et al, 2001,Chabowski, et al, 2004,Chen, Yang, Loux, Georgeson, & Harmon, 2006, and because CD36 is expressed on tissues important in fatty acid metabolism (heart, skeletal muscle, fat, and in pathological states, liver) this may imply an important role for CD36 in insulin resistance (see later). Regulation of CD36 expression can be mediated both pre-and post-transcription.…”

Section: Cd36 Regulationmentioning

confidence: 97%

CD36: Implications in cardiovascular disease

Febbraio

Silverstein

2007

The International Journal of Biochemistry & Cell Biology

213

215

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CD36 is a broadly expressed membrane glycoprotein that acts as a facilitator of fatty acid uptake, a signaling molecule, and a receptor for a wide range of ligands, including apoptotic cells, modified forms of low density lipoprotein, thrombospondins, fibrillar beta-amyloid, components of gram positive bacterial walls and malaria infected erythrocytes. CD36 expression on macrophages, dendritic and endothelial cells, and in tissues including muscle, heart, and fat, suggest diverse roles, and indeed, this is truly a multifunctional receptor involved in both homeostatic and pathologic conditions. Despite an impressive increase in our knowledge of CD36 functions, in depth understanding of the mechanistic aspects of this protein remains elusive. This review focuses on CD36 in cardiovascular disease-what we know, and what we have yet to learn.

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“…Hyperglycemia has been suspected of accelerating atherosclerosis in type 2 diabetes [7,8] . The effect of high glucose levels on the risk of cardiovascular events starts at glucose concentrations below the non-diabetic glucose range (<6.1 mmol/L), and glucose continues to exert its effects within the diabetic glucose range (>11.1 mmol/L) in an exponential fashion [2] .…”

Section: Introductionmentioning

confidence: 99%

Breviscapine inhibits high glucose-induced proliferation and migration of cultured vascular smooth muscle cells of rats via suppressing the ERK1/2 MAPK signaling pathway

Xue

et al. 2012

Acta Pharmacol Sin

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Aim: To investigate the influences of breviscapine, a flavonoid extracted from Erigeron breviscapus, on the proliferation and migration of vascular smooth muscle cells (VSMCs) cultured in a high glucose medium and the underlying mechanisms. Methods: VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats and cultured in vitro. Cell proliferation was evaluated using Counting Kit-8 cell viability assay. Cell migration was evaluated using transwell migration assay and in vitro scratch assay. The expression and activity of protein kinase C-β2 (PKC-β2), extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (p38), and JNK mitogen-activated protein kinase (JNK) were measured with Western blotting. Results: Exposure of VSMCs to a high glucose (25 mmol/L) medium significantly increased the proliferation and migration potential as compared to the control group. Pretreatment with breviscapine (65 µmol/L and 108 µmol/L) attenuated high glucose-enhanced proliferation and migration of VSMCs. Exposure of VSMCs to the high glucose medium activated both the PKC-β2 and ERK1/2 MAPK, but not the p38 and JNK MAPK. Pretreatment with breviscapine (65 µmol/L and 108 µmol/L) blocked high glucose-induced increase of the ERK1/2 activity, but not that of the PKC-β2 activity. Conclusion: Our study demonstrated that breviscapine ameliorates high glucose-induced proliferation and migration of VSMCs via inhibiting ERK1/2 MAPK signaling.

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A link between diabetes and atherosclerosis: Glucose regulates expression of CD36 at the level of translation

Cited by 227 publications

References 43 publications

IL‐13 induces expression of CD36 in human monocytes through PPARγ activation

IL‐13 induces expression of CD36 in human monocytes through PPARγ activation

CD36: Implications in cardiovascular disease

Breviscapine inhibits high glucose-induced proliferation and migration of cultured vascular smooth muscle cells of rats via suppressing the ERK1/2 MAPK signaling pathway

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