Specific monocyte adhesion to endothelial cells induced by oxidized phospholipids involves activation of cPLA2 and lipoxygenase

Huber, J.F.K.; Fürnkranz, Alexander; Bochkov, Valery N.; Patricia, Mary Kim; Lee, Hans C.; Hedrick, Catherine C.; Berliner, Judith A.; Binder, Bernd R.; Leitinger, Norbert

doi:10.1194/jlr.m500555-jlr200

Cited by 55 publications

(39 citation statements)

References 48 publications

(77 reference statements)

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“…[113][114] This effect of glucose is mimicked by minimally modified LDL or by specific oxidized phospholipids. [115][116][117] In human macrophages, elevated glucose has been shown to increase expression of the scavenger receptor and fatty acid transporter CD36, 118 an effect that is mimicked by oleate and linoleate. 119 -120 However, a similar effect of glucose on CD36 has not been found in peritoneal macrophages from mice.…”

Section: Do Glucose and Lipids Exert Independent Effects In Cultured mentioning

confidence: 99%

Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?

Kanter

Johansson

LeBoeuf

et al. 2007

Circulation Research

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Abstract-It is becoming increasingly clear that suboptimal blood glucose control results in adverse effects on large blood vessels, thereby accelerating atherosclerosis and cardiovascular disease, manifested as myocardial infarction, stroke, and peripheral vascular disease. Cardiovascular disease is accelerated by both type 1 and type 2 diabetes. In type 1 diabetes, hyperglycemia generally occurs in the absence of elevated blood lipid levels, whereas type 2 diabetes is frequently associated with dyslipidemia. In this review article, we discuss hyperglycemia versus hyperlipidemia as culprits in diabetes-accelerated atherosclerosis and cardiovascular disease, with emphasis on studies in mouse models and isolated vascular cells. Recent studies on LDL receptor-deficient mice that are hyperglycemic, but exhibit no marked dyslipidemia compared with nondiabetic controls, show that diabetes in the absence of diabetes-induced hyperlipidemia is associated with an accelerated formation of atherosclerotic lesions, similar to what is seen in fat-fed nondiabetic mice. These effects of diabetes are masked in severely dyslipidemic mice, suggesting that the effects of glucose and lipids on lesion initiation might be mediated by similar mechanisms. Recent evidence from isolated endothelial cells demonstrates that glucose and lipids can induce endothelial dysfunction through similar intracellular mechanisms. Analogous effects of glucose and lipids are also seen in macrophages. Furthermore, glucose exerts many of its cellular effects through lipid mediators. We propose that diabetes without associated dyslipidemia accelerates atherosclerosis by mechanisms that can also be activated by hyperlipidemia. (Circ Res. 2007;100:769-781.)

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Section: Do Glucose and Lipids Exert Independent Effects In Cultured mentioning

confidence: 99%

Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?

Kanter

Johansson

LeBoeuf

et al. 2007

Circulation Research

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show abstract

“…Cells were incubated for 24 hours with AngII (10 -7 M), losartan (10 -6 M), or peritoneal macrophages from renin +/+ or renin -/-mice placed in the lower chamber. Adhesion assays were performed as described by Huber et al (70). Briefly, THP-1 cells were stimulated by TNF-α (10 ng/ml) and then labeled with calcein AM (catalog no.…”

Section: Adhesion Assaymentioning

confidence: 99%

Renin inhibition reduces hypercholesterolemia-induced atherosclerosis in mice

Lü¹,

Rateri²,

Feldman³

et al. 2008

J. Clin. Invest.

142

186

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The role of the renin angiotensin system (RAS) in atherosclerosis is complex because of the involvement of multiple peptides and receptors. Renin is the rate-limiting enzyme in the production of all angiotensin peptides. To determine the effects of renin inhibition on atherosclerosis, we administered the novel renin inhibitor aliskiren over a broad dose range to fat-fed LDL receptor-deficient (Ldlr -/-) mice. Renin inhibition resulted in striking reductions of atherosclerotic lesion size in both the aortic arch and the root. Subsequent studies demonstrated that cultured macrophages expressed all components of the RAS. To determine the role of macrophage-derived angiotensin in the development of atherosclerosis, we transplanted renin-deficient bone marrow to irradiated Ldlr -/-mice and observed a profound decrease in the size of atherosclerotic lesions. In similar experiments, transplantation of bone marrow deficient for angiotensin II type 1a receptors failed to influence lesion development. We conclude that renin-dependent angiotensin production in macrophages does not act in an autocrine/paracrine manner. Furthermore, in vitro studies demonstrated that coculture with renin-expressing macrophages augmented monocyte adhesion to endothelial cells. Therefore, although previous work suggests that angiotensin peptides have conflicting effects on atherogenesis, we found that renin inhibition profoundly decreased lesion development in mice.

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“…Monocyte adhesion assays were performed according to previous reports (15,16). HUVECs (3 3 10 4 cells per well) were seeded in 48-well plates and cultured overnight.…”

Section: Monocyte Adhesion Assaymentioning

confidence: 99%

Sphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells

Lee

Kim

et al. 2011

The Journal of Immunology

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Sphingosylphosphorylcholine (SPC) is a component of high-density lipoprotein particles. We investigated the functional role of SPC in HUVECs. SPC stimulation induced production of the CCL2 chemokine in a PTX-sensitive G-protein–dependent manner. SPC treatment caused the activation of NF-κB and AP-1, which are essential for SPC-induced CCL2 production, and induced the activation of three MAPKs, ERK, p38 MAPK, and JNK. Inhibition of p38 MAPK or JNK by specific inhibitors caused a dramatic decrease in SPC-induced CCL2 production. The Jak/STAT3 pathway was also activated upon SPC stimulation of HUVECs. Pretreatment with a Jak inhibitor blocked not only SPC-induced p38 MAPK and JNK activation, but also NF-κB and AP-1 activation. Our results suggest that SPC stimulates HUVECs, resulting in Jak/STAT3–, NF-κB–, and AP-1–mediated CCL2 production. We also observed that SPC stimulated expression of the adhesion molecule ICAM-1 in HUVECs. Our results suggest that SPC may contribute to atherosclerosis; therefore, SPC and its unidentified target receptor offer a starting point for the development of a treatment for atherosclerosis.

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Specific monocyte adhesion to endothelial cells induced by oxidized phospholipids involves activation of cPLA2 and lipoxygenase

Cited by 55 publications

References 48 publications

Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?

Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?

Renin inhibition reduces hypercholesterolemia-induced atherosclerosis in mice

Sphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells

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