The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by interferon γ

Wågsäter, Dick; Olofsson, Peder S.; Norgren, Lars; Stenberg, Björn; Sirsjö, Allan

doi:10.1016/j.bbrc.2004.10.160

Cited by 83 publications

(59 citation statements)

References 19 publications

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“…This receptor has been confirmed to be expressed in lipid-laden macrophages and SMCs in human atherosclerotic lesions. 40,41 Regulation of CXCL16 expression by IFN-␥ has been detected in vitro in human aortic SMCs and monocytes. 8,40 Genetic disruption of any of scavenger receptor SR-A or CD36 results in a significant decrease in lesion formation, suggesting that these 2 receptors play a crucial role in the development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…40,41 Regulation of CXCL16 expression by IFN-␥ has been detected in vitro in human aortic SMCs and monocytes. 8,40 Genetic disruption of any of scavenger receptor SR-A or CD36 results in a significant decrease in lesion formation, suggesting that these 2 receptors play a crucial role in the development of atherosclerosis. 42,43 Although IFN-␥ is well-known as a proathero-genic cytokine, it has been reported that IFN-␥ downregulates expression of SR-A and CD36.…”

Section: Discussionmentioning

confidence: 99%

“…This paradox could now be explained by the findings that IFN-␥ upregulates expression of CXCL16 in vivo in lesions and in monocytes and SMCs in vitro. 40,8 IFN-␥ also enhances the uptake of oxidized low-density lipoprotein in monocytes and SMCs via the CXCL16 receptor. 40,8 Our present data have shown that an increased IFN-␥ level was paralleled with a significant elevation of CXCL16 mRNA expression in both lesions and spleens after IL-18 administration.…”

Section: Discussionmentioning

confidence: 99%

“…40,8 IFN-␥ also enhances the uptake of oxidized low-density lipoprotein in monocytes and SMCs via the CXCL16 receptor. 40,8 Our present data have shown that an increased IFN-␥ level was paralleled with a significant elevation of CXCL16 mRNA expression in both lesions and spleens after IL-18 administration. This suggests that the proatherogenic role of IL-18 could partly depend on IFN-␥ mediated upregulation of CXCL16.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, two studies have recently shown that IL-18 can induce CXCL16 in SMCs. 46,40 However, no experiment shows a direct effect of IL-18 on CXCL16 expression in the absence of IFN-␥ in either SMCs or macrophages.…”

Section: Discussionmentioning

confidence: 99%

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IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-γ and CXCL16 Expression Independently of T Cells

Tenger

Sundborger

Jawień

et al. 2005

ATVB

118

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Objective-The proatherogenic effect of IL-18 is shown to be dependent on IFN-␥ production. It is believed that activated T cells play a proatherogenic role through secretion of IFN-␥. However, recent studies in vitro have shown that macrophages, NK cells, and even vascular smooth muscle cells may also secrete IFN-␥ after stimulation by cytokines like IL-18. We therefore investigated whether cells other than activated T cells can play a proatherogenic role via IFN-␥ secretion under the stimulation of IL-18 in vivo. Methods and Results-SCID/apoE knockout mice were injected intraperitoneally with either IL-18 or phosphate-buffered saline 3 times per week for 7 weeks. Our results show that administration of IL-18 leads to 3-fold larger lesions and 2-fold higher circulating IFN-␥ despite the absence of T cells. In addition, increased IFN-␥, accompanied by elevation of the scavenger receptor/chemokine CXCL16, was observed in both lesions and spleens.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-γ and CXCL16 Expression Independently of T Cells

Tenger

Sundborger

Jawień

et al. 2005

ATVB

118

View full text Add to dashboard Cite

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Scavenger Receptors: Structure, Function and Diversity

Stephen

Ponnambalam

2012

Encyclopedia of Life Sciences

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Scavenger receptors (SRs) form an increasingly important group of cell surface receptors that bind and internalise a variety of ligands. These membrane‐bound receptors were initially classified within this group on the basis of their ability to bind to modified low‐density lipoprotein (LDL) particles and as of date, at least 17 members of this family, organised into eight families, have been identified in nematodes, arthropods and higher organisms. Members of the SR family play key roles in many pathological conditions including pattern recognition in immune responses, pathogen infection and in the development and progression of atherosclerosis. The uptake of modified lipid particles by SRs in macrophages can lead to the formation of foam cells. Perturbation in the levels of some SRs can enhance or reduce the risk of cardiovascular disease. In this review, we describe the well‐characterised members of this group of proteins and discuss the functional and biological roles of these proteins in animal health and disease. Key Concepts: SR family contains membrane bound and soluble proteins. SRs bind to a variety of ligands including lipoproteins, carbohydrates and proteoglycans. SRs seem to play an important role in innate immunity against bacteria, with the lack of certain SRs leading to fatal susceptibility to infection. The malarial parasite and viruses may also exploit SR function to infect cells. SRs expressed in macrophages and endothelial cells bind to modified LDL particles to initiate atherosclerosis. The binding of modified LDL to SRs result in signalling cascades inside the cells, which may result in apoptosis. Knockdown of specific SRs or overexpression can reduce atherosclerosis incidence. SRs may also be involved in tumour metastasis.

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Gamma interferon: a central mediator in atherosclerosis

2005

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Atherosclerosis is a chronic inflammatory disease of the vasculature with lesions developing in the arterial wall, frequently in the coronary and carotid arteries. The interaction between macrophages and lymphocytes within the atherosclerotic lesion microenvironment exemplifies a site where both innate and adaptive immunity contribute towards disease progression. As gamma interferon (IFN-gamma), the classic macrophage activating factor, has been localized to atherosclerotic lesions, this review will focus on its contribution to plaque pathology and will finally consider how current therapies, as exemplified by HMG CoA reductase inhibitors or statins, may impact this process beyond lipid lowering, in part by inhibiting IFN-gamma dependent processes. IFN-gamma sources within the atheroma as well as receptors, signaling pathways and its effects on macrophages as well as on vascular smooth muscle and endothelial cells will be considered. Therapeutic interventions targeting molecular events associated with IFN-gamma signaling offer novel approaches to the treatment of atherosclerosis.

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The chemokine and scavenger receptor CXCL16/SR-PSOX is expressed in human vascular smooth muscle cells and is induced by interferon γ

Cited by 83 publications

References 19 publications

IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-γ and CXCL16 Expression Independently of T Cells

IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-γ and CXCL16 Expression Independently of T Cells

Scavenger Receptors: Structure, Function and Diversity

Gamma interferon: a central mediator in atherosclerosis

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