Monocyte-Macrophage Participation in Atherogenesis: Inflammatory Components of Pathogenesis

Schwartz, Colin J.; Valente, Anthony J.; Sprague, Eugene A.; Kelley, Jim; Suenram, C. Alan; Graves, Dana T.; Rozek, Marius M.; Edwards, Ellen H.; Delgado, Ruby

doi:10.1055/s-2007-1003539

Cited by 58 publications

(18 citation statements)

References 16 publications

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“…Other factors found to regulate MCP-1 expression that may play a role include growth factors and the inflammatory cytokines (11). In addition, other components of recruitment are likely to involve hemodynamic factors, plasma proteins, and local generation of cytokines, permeability factors, and cell adhesion molecules (26,27 arteries with fatty streaks may be due to the fact that they did not examine patients with progressive coronary artery disease. These authors also did not detect MCP-1 expression in vascular SMCs of rabbits with diet-induced hypercholesterolemia.…”

Section: Resultsmentioning

confidence: 99%

Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

Dluz

Graves

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

192

106

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Atherosclerosis is marked by an overt inflammatory infiltrate, with enhanced recruitment of monocytes/macrophages observed in both human and experimental atherosclerosis. We previously determined that monocyte chemoattractant protein 1 (MCP-1) accounts for virtually all of the chemotactic activity produced by vascular (aortic) smooth muscle cells in culture. We now report that arteries from a primate model of atherosclerosis with dietary-induced hypercholesterolemia exhibit increased levels of MCP-1 mRNA expression in vivo, whereas their normal counterparts demonstrate minimal MCP-1 expression. Furthermore, immunohistochemistry and in situ hybridization clearly indicate that the expression of MCP-1 protein and mRNA is in the smooth muscle cells of the medial layer of the artery and in monocytelike and smooth muscle-like cells found in the overlying intimal lesion. These studies indicate that one of the responses to dietary hypercholesterolemia is the expression of MCP-1 by vascular smooth muscle cells. This expression, when augmented with other cellular and molecular factors, could significantly contribute to the recruitment of monocytes/macrophages to the vessel wall.Atherosclerosis is a multistage disease involving invasion of the intima by smooth muscle cells (SMCs) from the media, followed by SMC proliferation and production of an extensive insoluble matrix including such connective tissue components as collagens, elastin, and proteoglycans (1). The two major lesions seen are the fatty streak and the atheromatous or fibrotic plaque. Evidence suggests that fatty streaks, seen in childhood, may progress to fibrotic lesions in adults. Both types of lesions are typified by macrophage invasion (2). Factors released by the macrophage have been shown to influence SMC migration, proliferation, and connective tissue gene expression (3-5). Thus a renewed appreciation of the role of the inflammatory process in coronary arteriosclerosis has emerged.Monocyte chemoattractant protein 1 (MCP-1) is a monomeric polypeptide that migrates in a gel with an estimated molecular mass of 9-15 kDa (6, 7). The various forms of MCP-1 result from differences in O-linked glycosylation and do not affect chemotactic activity (8, 9). Unlike other chemoattractants, MCP-1 is relatively specific for monocytes. Lymphocytes and polymorphonuclear leukocytes lack MCP-1 receptors and do not respond to MCP-1 (10). Previous in vitro studies have shown that this protein can either be secreted by normal cells such as endothelial cells (11) and SMCs (12) or by many tumor cell lines (6, 13). MCP-1 expression in most normal cell types occurs in response to proinflammatory factors such as interleukin 1, tumor necrosis factor a, and interferon y (11, 14). It has also been shown that minimally modified plasma low density lipoprotein stimulates MCP-1 production by human SMCs and endothelial cells in vitro (15). It has been suggested that macrophage/ monocyte recruitment in atherosclerosis occurs in response to a gradient of chemoattractants released ...

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Section: Resultsmentioning

confidence: 99%

Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

Dluz

Graves

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

192

106

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“…The key role of macrophages derived from blood-borne monocytes in inflammatory diseases and particularly in atherosclerosis development has been well documented (1)(2)(3). A property that can be considered essential for monocytes/macrophages to exert their roles is their ability to emigrate from the circulating blood pool into different tissues or structures.…”

Section: From the Epi 99 -36 Laboratoire D'hématologie Faculté De Mmentioning

confidence: 99%

Inhibition of p70S6 Kinase during Transforming Growth Factor-β1/Vitamin D3-induced Monocyte Differentiation of HL-60 Cells Allows Tumor Necrosis Factor-α to Stimulate Plasminogen Activator Inhibitor-1 Synthesis

Peiretti¹,

Lopez²,

Deprez-Beauclair³

et al. 2001

Journal of Biological Chemistry

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We investigated intracellular mechanisms involved in the up-regulation of plasminogen activator inhibitor I (PAI-1) synthesis by human recombinant tumor necrosis factor-␣ (TNF) during monocyte differentiation of HL-60 cells triggered by the transforming growth factor-␤1/ vitamin D 3 (TGF/D3) mixture. TGF/D3-treated cells expressed surface monocytic markers and produced noticeable amounts of PAI-1 but stopped to proliferate. A reduced p70 S6 kinase (p70 S6K ) phosphorylation was also observed and, in this situation, TNF dramatically enhanced PAI-1 synthesis. Similarly, TNF significantly up-regulated PAI-1 synthesis when p70 S6K phosphorylation was inhibited by rapamycin. This phenomenon was not due to a general decrease in protein synthesis but involved the activation of gene transcription rather than PAI-1 mRNA stabilization. The level of the transcriptional regulator factor E2F1, a repressor of PAI-1 gene expression, was shown to be down-modulated in TGF/D3-as well as in rapamycin-treated cells. Furthermore, the apoptotic effect of TNF in HL-60 cells appeared to be prevented by the addition of either TGF/D3 or rapamycin. In conclusion, these results indicate that inhibition of p70 S6K phosphorylation during TGF/D3-induced monocyte differentiation of HL-60 cells is a determinant factor that allows TNF to exert its up-regulating effect on PAI-1 synthesis while protecting cells from apoptosis.

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“…Monocyte recruitment plays a vital role in atherogenesis (24) and may be mediated through processes which include "endothelial activation," in which the cytokines such as interleukin I and tumor necrosis factor can generate the synthesis ofendothelial leukocyte adhesion molecules, otherwise known as ELAMS (1). There are, of course, many components to inflammatory monocyte recruitment, other than ELAMS, and these are discussed subsequently in more detail when the exogenous cells of the arterial wall are reviewed; That arterial endothelial cells (EC) can recognize and transduce fluid mechanical signals, such as shear stress, is of considerable biologic interest.…”

Section: The Endogenous Cells Of the Arterial Wallmentioning

confidence: 99%

Cellular Mechanisms in the Response of the Arterial Wall to Injury and Repair

et al. 1989

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This synopsis emphasizes the inappropriateness of a "single stimulus-single response" approach in understanding the response of the arterial wall to injury and repair. The outcome of any injurious stimulus is a series of interactive cascades among the endogenousand exogenous cellular and non-cellular components of the arterial wall, and the cellular and non-cellular elements of the blood. Both genetic and hemodynamic factors can further influencethis response. The more prominent of the cellular and non-cellular components have beendiscussed.These include: I) the vascularendothelium, its dynamic interaction with macromolecules and formed elements of the blood, its role in the transport of plasma proteins, its influenceon the function of arterial smooth muscle cellsand the recruitment of blood-born monocytes; 2) the arterial smooth muscle cell, its role in the vasomotor function of the artery wall, arterial repair and reconstruction, metabolism of lipids and the secretion of cytokines regulating monocyte recruitment; 3) the mononuclear phagocyte, its role in arterial debridement, metabolism of modified LDLs, a precursor of the cholesteryl ester-rich foam cell, and the secretion of neutral hydrolases, bioactive lipids and cytokines; 4) lymphocytes, as mediators of the inflammatoryresponseand possibleautoimmune reactions;5)platelets, their rolesin hemostasis,thrombosis, atherogenesis, and the repair processand 6) plasma LDLs, their oxidative modification by cells of the vessel walland their roles in the injury process.The interactive processes among arterial and circulatingcomponents in both injury and repair is emphasized.

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Monocyte-Macrophage Participation in Atherogenesis: Inflammatory Components of Pathogenesis

Cited by 58 publications

References 16 publications

Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

Inhibition of p70S6 Kinase during Transforming Growth Factor-β1/Vitamin D3-induced Monocyte Differentiation of HL-60 Cells Allows Tumor Necrosis Factor-α to Stimulate Plasminogen Activator Inhibitor-1 Synthesis

Cellular Mechanisms in the Response of the Arterial Wall to Injury and Repair

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