Prevention of increased monocyte adhesiveness in smokers after vitamin C intake

Weber, C. W.; Weber, Katharina; Erl, W.; Weber, Pavel

doi:10.1016/0021-9150(95)96473-6

Cited by 12 publications

(12 citation statements)

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“…Statins also exert beneficial effects that are independent of their lipidlowering properties (37)(38)(39). Statins improve endothelial function; stabilize atherosclerotic plaques; and inhibit platelet aggregation, vascular SMC proliferation, and vessel wall inflammation (27, 28, 33-36, 40 -42).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-18-induced Human Coronary Artery Smooth Muscle Cell Migration Is Dependent on NF-κB- and AP-1-mediated Matrix Metalloproteinase-9 Expression and Is Inhibited by Atorvastatin

Chandrasekar

Mummidi

Mahimainathan

et al. 2006

Journal of Biological Chemistry

188

189

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Atherosclerosis is considered to be a chronic inflammatory disease characterized by enhanced expression of proinflammatory cytokines, chemokines, and adhesion molecules (1-3). The cross-talk between cytokines, chemokines, and infiltrating immune cells amplifies the inflammatory cascade in the vessel wall, resulting in atherogenesis (1-3).Interleukin-18 (IL-18) 3 is a proinflammatory and proatherogenic cytokine that induces the expression of other proinflammatory cytokines and adhesion molecules (4). IL-18 has been localized to human atherosclerotic lesions (5, 6), and circulating IL-18, which is increased in acute coronary syndromes (7), has been shown to predict future cardiovascular events (7). A positive correlation between serum IL-18 levels and carotid intima-media thickness has been demonstrated (8). Administration of IL-18 aggravates atherosclerosis in mice (9). Moreover, atherogenesis is reduced in IL-18-deficient apoE knock-out mice (10), suggesting a causal role for IL-18 in the development and progression of atherosclerosis.Recently, we demonstrated that IL-18 induces human aortic smooth muscle cell (SMC) proliferation (11). However, it is not known whether IL-18 induces SMC migration. Both migration and proliferation play a role in normal and diseased vessels (1-3). SMC migration contributes to normal angiogenesis. However, SMC migration also plays a causal role in pathological remodeling of the vessel walls during atherosclerosis, arteriosclerosis, and restenosis following angioplasty (1-3).Vessel wall remodeling is characterized by a disruption in the delicate balance between extracellular matrix (ECM) deposition and degradation, with matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of matrix metalloproteinases (TIMPs)) playing a prominent role. MMPs are zinc-dependent proteases and are classified as collagenases, stromelysins, elastases, and gelatinases based on substrate specificity. Their expression is regulated at both the transcriptional and post-transcriptional levels. They are synthesized as proenzymes and are activated following proteolytic cleavage. SMCs express MMP2 (gelatinase A) and MMP9 (gelatinase B), the two gelatinases described so far (12). Excess activation of MMP2 and MMP9, without alteration of TIMP expression and activation, results in destruction of the ECM and can lead to pathological remodeling and vascular restenosis (12-15). Because increased matrix degradation promotes SMC migration (15), we hypothesized that IL-18 induces SMC migration via induction of MMP9. Our novel findings demonstrate that IL-18 promotes SMC

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Section: Discussionmentioning

confidence: 99%

Interleukin-18-induced Human Coronary Artery Smooth Muscle Cell Migration Is Dependent on NF-κB- and AP-1-mediated Matrix Metalloproteinase-9 Expression and Is Inhibited by Atorvastatin

Chandrasekar

Mummidi

Mahimainathan

et al. 2006

Journal of Biological Chemistry

188

189

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“…Due to the invasive nature of such techniques, this approach will demand preparations with an extended duration of action or therapeutics that have a lasting effect on atherogenesis or restenosis even with a single dosage regimen. Viral expression vectors may be used in achieving prolonged up-regulation of anti-inflammatory interleukins, such as (v)IL-10 ( Kim et al, 2000a;Minter et al, 2001;von der Thü sen et al, 2001a), interleukin antagonists, such as IL-1ra and soluble TNF receptor (Giannoukakis et al, 1999;Kim et al, 2001), inhibitors of NF-B signaling, such as IB␣ (Wrighton et al, 1996;Bondeson et al, 1999;Weber et al, 1999), and antisense oligonucleotides and ribozymes directed against proinflammatory interleukins and interleukin-induced genes. Although ex-tended transgene expression has been found to occur with some adenoviruses, including Ad-IL-10 (Ͼ200 days, unpublished data), the use of AAVs or Ad/AAV hybrids may be preferable in accomplishing this goal (Lynch et al, 1997;Recchia et al, 1999;Monahan and Samulski, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…The recognition of the physiological importance of this inhibitory pathway has prompted the evaluation of the anti-atherogenic properties of IB␣ administration. Adenoviral transfer of IB␣ has thus been found to effect down-regulation of inflammatory genes in endothelial cells, including VCAM-1, IL-1, IL-6, and IL-8 (Wrighton et al, 1996), and to lead to inhibition of monocyte adhesion and transmigration on TNF␣-activated endothelium (Weber et al, 1999). In addition, TNF␣-induced endothelial expression of adhesion molecules (E-selectin and ICAM-1) and chemokines (MCP-1) is attenuated by retrovirus-mediated introduction of a proteolysis-resistant IB␣ mutant, IB⌬N, and the addition of pharmacological inhibitors of IB␣ phosphorylation and proteasome degradation (Cobb et al, 1996;Pierce et al, 1997;Lockyer et al, 1998;Hipp et al, 2002).…”

Section: G Inhibition Of Interleukin-induced Gene Expressionmentioning

confidence: 99%

Interleukins in Atherosclerosis: Molecular Pathways and Therapeutic Potential

et al. 2003

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“…There is evidence that oxidized lipids, primarily derived from low density lipoproteins (LDL), 1 contribute to all stages of atherosclerotic development (5)(6)(7)(8). Initially, they facilitate monocyte deposition within the subendothelial space by stimulating endothelial cells to express monocyte-specific adhesion molecules (9,10) and secrete monocyte chemoattractants (11,12). Later, highly oxidized lipids such as malondialdehyde and 4-hydroxynonenal modify the protein component of LDL so that it is recognized by the macrophage scavenger/ oxidized LDL receptor rather than the native LDL receptor (13)(14)(15).…”

mentioning

confidence: 99%

Structural Identification of a Novel Pro-inflammatory Epoxyisoprostane Phospholipid in Mildly Oxidized Low Density Lipoprotein

Watson¹,

Subbanagounder²,

Welsbie³

et al. 1999

Journal of Biological Chemistry

207

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One of the earliest steps in the development of the atherosclerotic lesion is the accumulation of monocyte/ macrophages within the vessel wall. Oxidized lipids present in minimally modified-low density lipoproteins (MM-LDL) contribute to this process by activating endothelial cells to express monocyte-specific adhesion molecules and chemoattractant factors. A major focus of our group has been the isolation and characterization of the biologically active oxidized lipids in MM-LDL. We have previously characterized three oxidized phospholipids present in MM-LDL, atherosclerotic lesions of fat fed rabbits, and autoxidized 1-palmitoyl-2-arachidonoyl-snglycero-3-phosphocholine (Ox-PAPC) that induced human aortic endothelial cells to adhere human monocytes in vitro. We have used sequential normal and reverse phase-high performance liquid chromatography to isolate various isomers of an oxidized phospholipid from autoxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine. The fatty acid in the sn-2 position of this biologically active isomer and its dehydration product was released by phospholipase A 2 and characterized. Hydrogenation with platinum(IV) oxide/hydrogen suggested a cyclic moiety, and reduction with sodium borohydride suggested two reducible oxygencontaining groups in the molecule. The fragmentation pattern produced by electrospray ionization-collision induced dissociation-tandem mass spectrometry was consistent with a molecule resembling an E-ring prostaglandin with an epoxide at the 5,6 position. The structure of this lipid was confirmed by proton nuclear magnetic resonance spectroscopy analysis of the free fatty acid isolated from the dehydration product of m/z 828.5. Based on these studies, we arrived at the structure of the biologically active oxidized phospholipids as 1-palmitoyl-2-(5,6-epoxyisoprostane E 2 )-sn-glycero-3-phosphocholine. The identification of this molecule adds epoxyisoprostanes to the growing list of biologically active isoprostanes.

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Prevention of increased monocyte adhesiveness in smokers after vitamin C intake

Cited by 12 publications

References 0 publications

Interleukin-18-induced Human Coronary Artery Smooth Muscle Cell Migration Is Dependent on NF-κB- and AP-1-mediated Matrix Metalloproteinase-9 Expression and Is Inhibited by Atorvastatin

Interleukin-18-induced Human Coronary Artery Smooth Muscle Cell Migration Is Dependent on NF-κB- and AP-1-mediated Matrix Metalloproteinase-9 Expression and Is Inhibited by Atorvastatin

Interleukins in Atherosclerosis: Molecular Pathways and Therapeutic Potential

Structural Identification of a Novel Pro-inflammatory Epoxyisoprostane Phospholipid in Mildly Oxidized Low Density Lipoprotein

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