Expression Of Scavenger Receptor CD36 Research Articles

Interaction of monocytes with vascular smooth muscle cells regulates monocyte survival and differentiation through distinct pathways.

Vascular smooth muscle cells (VSMCs) may regulate monocyte functions within atherosclerotic lesions. We investigated the impact of VSMC/monocyte interactions on monocyte apoptosis and scavenger receptor CD36 expression, key events related to monocyte survival and differentiation. Serum deprivation significantly increased THP-1 and human peripheral blood monocyte apoptosis. However, this was significantly reversed by physical binding to human VSMCs (HVSMCs). On binding to HVSMCs, antiapoptotic kinase Akt and its downstream targets were phosphorylated, and Bcl-2 expression was enhanced. Binding-mediated suppression of apoptosis and Akt phosphorylation were attenuated by a phosphoinositide 3-kinase inhibitor and also by an antibody to vascular cell adhesion molecule-1. CD36 expression was also significantly increased in THP-1 cells and in human peripheral blood monocytes after binding to HVSMCs, and this was mediated by both direct contact and soluble factors. Extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase phosphorylation was increased in THP-1 cells after HVSMC coculture. Furthermore, an ERK1/2 inhibitor blocked monocyte CD36 upregulation. Contact-dependent CD36 induction and ERK1/2 phosphorylation in monocytes were inhibited by blocking vascular cell adhesion molecule-1 on HVSMC, whereas soluble factor-induced CD36 expression was attenuated by a monocyte chemoattractant protein-1 neutralizing antibody. These data provide evidence of novel VSMC-dependent local regulation mechanisms for monocyte survival and differentiation in atherosclerosis.

High glucose concentrations stimulate human monocyte sodium/hydrogen exchanger activity and modulate atherosclerosis-related functions.

In the present study, the effect of high (20 mM) glucose concentrations on human monocyte sodium/hydrogen exchanger (NHE1) activity, scavenger receptor CD36 expression, cell adhesion, and cell migration have been investigated. Incubation with high glucose concentrations caused an increase in NHE1 activity, as estimated by internal pH and sodium-uptake measurements. This effect was specific for glucose, since it was not observed when monocytes were incubated in the presence of 20 mM of galactose, fructose, or mannitol. In addition, the activation of sodium uptake was inhibited by ethylisopropyl amiloride (EIPA), phloretine and cytochalasine B, and calphostin C. High glucose concentrations also increased the expression of CD36 receptors on the surface of monocytes and positively influenced monocyte migration and adhesion to laminin. EIPA added together with glucose counteracted these effects. The data of the present study suggest that a high glucose concentration can influence atherosclerosis-related monocyte functions via NHE1 activation.

Microarray analysis of peroxisome proliferator-activated receptor-γ induced changes in gene expression in macrophages

We used a combination of expression microarray and Northern blot analyses to identify target genes for peroxisome proliferator-activated receptor (PPAR) γ in RAW264.7 macrophages. PPARγ natural ligand 15-deoxy-Δ 12,14 prostaglandin and synthetic ligands ciglitazone and rosiglitazone increased the expression of scavenger receptor CD36 and ATP-binding cassette transporter A1, as well as adipophilin (a lipid droplet coating protein involved in intracellular lipid storage and transport), calpain (a protease implicated in ABCA1 protein degradation), and ADAM8 (a disintegrin and metalloprotease protein involved in cell adhesion). These findings are relevant to understanding the effect of PPARγ activation on gene expression and cognate pathways in macrophages.

CD36 scavenger receptor expression and oxLDL uptake are inhibited by vitamin E

Conference Abstract| October 01 2000 CD36 scavenger receptor expression and oxLDL uptake are inhibited by vitamin E R. Ricciarelli; R. Ricciarelli 1Büblstrasse, 28 3012 Bern Switzerland Search for other works by this author on: This Site PubMed Google Scholar T. M. Zingg; T. M. Zingg 1Büblstrasse, 28 3012 Bern Switzerland Search for other works by this author on: This Site PubMed Google Scholar A. Azzi A. Azzi 1Büblstrasse, 28 3012 Bern Switzerland Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2000) 28 (5): A242. https://doi.org/10.1042/bst028a242a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation R. Ricciarelli, T. M. Zingg, A. Azzi; CD36 scavenger receptor expression and oxLDL uptake are inhibited by vitamin E. Biochem Soc Trans 1 October 2000; 28 (5): A242. doi: https://doi.org/10.1042/bst028a242a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu nav search search input Search input auto suggest search filter All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2000 Biochemical Society2000 Article PDF first page preview Close Modal You do not currently have access to this content.

Vitamin E reduces the uptake of oxidized LDL by inhibiting CD36 scavenger receptor expression in cultured aortic smooth muscle cells.

Vitamin E is well known as an antioxidant, and numerous studies suggest that it has a preventive role in atherosclerosis, although the mechanism of action still remains unclear. The original aim of this study was to establish whether alpha-tocopherol (the most active form of vitamin E) acts at the earliest events on the cascade of atherosclerosis progression, that of oxidized LDL (oxLDL) uptake and foam-cell formation. We show here that the CD36 scavenger receptor (a specific receptor for oxLDL) is expressed in cultured human aortic smooth muscle cells (SMCs). Treatment of SMCs and HL-60 macrophages with alpha-tocopherol (50 micromol/L, a physiological concentration) downregulates CD36 expression by reducing its promoter activity. Furthermore, we find that alpha-tocopherol treatment of SMCs leads to a reduction of oxLDL uptake. This study indicates that CD36 is expressed in cultured human SMCs. In these cells, CD36 transports oxLDL into the cytosol. alpha-Tocopherol inhibits oxLDL uptake by a mechanism involving downregulation of CD36 mRNA and protein expression. Therefore, the beneficial effect of alpha-tocopherol against atherosclerosis can be explained, at least in part, by its effect of lowering the uptake of oxidized lipoproteins, with consequent reduction of foam cell formation.

Expression of macrophage scavenger receptors in various human tissues and atherosclerotic lesions

Expression of CD36 scavenger receptors on macrophages is involved in oxidized low-density lipoprotein (OxLDL) uptake and foam cell formation during atherosclerotic lesion development. It has been shown previously in vitro and in vivo that the atherosclerotic risk factor homocysteine (Hcy) stimulates macrophage CD36 expression and OxLDL uptake. We now examined the effects of aged garlic extract (AGE), a garlic preparation enriched in water-soluble organic sulfur-containing compounds, on Hcy-induced CD36 expression and foam cell formation in human monocytes/macrophages.Incubation with Hcy (200 μM for 72 h) in THP-1-derived macrophages and primary human macrophages caused a 37.8 ± 5.2% and 60.7 ± 4.2% increase in CD36 expression compared to control, respectively. Coincubation with AGE (5 mg/ml) significantly suppressed CD36 expression in THP-1 derived macrophages by 48.6 ± 9.0% compared to Hcy-incubated cells only. AGE (1–5 mg/ml) dose dependently inhibited Hcy-induced CD36 expression in primary human macrophages, and decreased binding of nuclear proteins to a PPARγ response element. Preincubation with AGE significantly inhibited DiI-labeled OxLDL uptake.These data indicate that AGE inhibits CD36 expression and OxLDL uptake in human macrophages by modulating the PPARγ pathway, and suggest that the extract could be useful for the prevention of atherosclerotic lesions.