Atherosclerosis as an Inflammatory Process

Schwartz, Colin J.; Valente, Anthony J.; Sprague, Eugene A.; Kelley, Jim; Suenram, C. Alan; Rozek, Marius M.

doi:10.1111/j.1749-6632.1985.tb11849.x

Cited by 52 publications

(12 citation statements)

References 13 publications

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“…Furthermore, we identified that ALCAM expression was up-regulated in the atherosclerotic aorta from apo-E knock-out mouse (data not shown). Given that inflammation plays crucial roles in atherosclerosis, ALCAM and sALCAM may play particular roles in the development of atherosclerosis (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Molecular Isolation and Characterization of a Soluble Isoform of Activated Leukocyte Cell Adhesion Molecule That Modulates Endothelial Cell Function

Ikeda

Quertermous

2004

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Molecular Isolation and Characterization of a Soluble Isoform of Activated Leukocyte Cell Adhesion Molecule That Modulates Endothelial Cell Function

Ikeda

Quertermous

2004

Journal of Biological Chemistry

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“…In the past decade, many reports have suggested that hyperinsulinemia associated with insulin resistance might be a risk factor in atherosclerotic diseases such as coronary heart disease (9 -11), which is one of the major causes of death in such patients (34). Macrophages play an important role in the initial stages of atherosclerosis by taking up modified low density lipoprotein, which is accompanied by a morphological change into foam cells and secretion of various cytokines (4,35,36). In addition, many cholesterol-enriched foam cells have been observed to be a characteristic aspect of the developed atherosclerotic lesions (6).…”

Section: Discussionmentioning

confidence: 99%

Insulin Up-regulates Tumor Necrosis Factor-α Production in Macrophages through an Extracellular-regulated Kinase-dependent Pathway

Iida¹,

Shimano²,

Kawakami³

et al. 2001

Journal of Biological Chemistry

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Hyperinsulinemia has recently been reported as a risk factor for atherosclerotic diseases such as coronary heart disease; however, the effect of insulin on the development of atherosclerosis is not well understood. Here we have investigated the direct effect of insulin on macrophages, which are known to be important in the atherosclerotic process. We treated THP-1 macrophages with insulin (10 ؊7 M) and examined the gene expression using nucleic acid array systems. The results of array analysis showed that insulin stimulated gene expression of tumor necrosis factor-␣ (TNF-␣) the most among all genes in the analysis. In addition, insulin administration to macrophages enhanced both mRNA expression and protein secretion of TNF-␣ in a dose-dependent manner. To determine the signaling pathway involved in this TNF-␣ response to insulin, we pretreated the cells with three distinct protein kinase inhibitors: wortmannin, PD98059, and SB203580. Only PD98059, which inhibits extracellular signal-regulated kinases, suppressed insulin-induced production of TNF-␣ mRNA and protein in THP-1 macrophages. These observations indicate that insulin stimulates TNF-␣ production in macrophages by regulating the expression of TNF-␣ mRNA and that the extracellular signal-regulated kinase signaling pathway may have a critical role in stimulating the production of TNF-␣ in response to insulin in macrophages.

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“…Macrophages are mediators of inflammation in the vasculature and participate in the development of atherosclerotic plaques [Schwartz et al, 1985]. In the pathogenesis of atherosclerosis, PPARα activation could result initially in reduced leukocyte adhesion to activated endothelial cells of the arterial lumen, and subsequently in inhibiting the formation of macrophage foam cells by regulating expression of genes involved in reverse cholesterol transport and reactive oxygen species output [Chinetti et al, 2001; Zandbergen and Plutzky, 2007].…”

Section: Pparα Functionsmentioning

confidence: 99%

PPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer

et al. 2010

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The peroxisome proliferator-activated receptor α (PPARα, or NR1C1) is a nuclear hormone receptor activated by a structurally diverse array of synthetic chemicals known as peroxisome proliferators. Endogenous activation of PPARα in liver has also been observed in certain gene knockout mouse models of lipid metabolism, implying the existence of enzymes that either generate (synthesize) or degrade endogenous PPARα agonists. For example, substrates involved in fatty acid oxidation can function as PPARα ligands. PPARα serves as a xenobiotic and lipid sensor to regulate energy combustion, hepatic steatosis, lipoprotein synthesis, inflammation and liver cancer. Mainly, PPARα modulates the activities of all three fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal ω-oxidation, and thus plays a key role in energy expenditure. Sustained activation of PPARα by either exogenous or endogenous agonists leads to the development of hepatocellular carcinoma resulting from sustained oxidative and possibly endoplasmic reticulum stress and liver cell proliferation. PPARα requires transcription coactivator PPAR-binding protein (PBP)/mediator subunit 1(MED1) for its transcriptional activity.

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Atherosclerosis as an Inflammatory Process

Cited by 52 publications

References 13 publications

Molecular Isolation and Characterization of a Soluble Isoform of Activated Leukocyte Cell Adhesion Molecule That Modulates Endothelial Cell Function

Molecular Isolation and Characterization of a Soluble Isoform of Activated Leukocyte Cell Adhesion Molecule That Modulates Endothelial Cell Function

Insulin Up-regulates Tumor Necrosis Factor-α Production in Macrophages through an Extracellular-regulated Kinase-dependent Pathway

PPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer

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