Expression of monocyte chemotactic protein and interleukin-8 by cytokine-activated human vascular smooth muscle cells.

Wang, Ji Ming; Sica, Antonio; Peri, Giuseppe; Walter, Sabine; Padura, Ines Martin; Libby, Peter; Ceska, M.; Lindley, I. J. D.; Colotta, Francesco; Mantovani, Alberto

doi:10.1161/01.atv.11.5.1166

Cited by 172 publications

(85 citation statements)

References 38 publications

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“…Thus, chemokines play a pivotal role in the development and complication of atheroma. Modified LDL and pro-inflammatory cytokines such as TNF␣, IL-1␤, IFN␥, or CD40 ligand induce chemokine expression in cells found in atheroma, such as EC, SMC, and M⌽ (31)(32)(33). However, knowledge of potential endogenous inhibitory mechanisms has lagged behind understanding of pro-inflammatory stimuli.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Takayama¹,

García‐Cardeña

Sukhova³

et al. 2002

Journal of Biological Chemistry

306

272

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Pro-inflammatory pathways participate in the pathogenesis of atherosclerosis. However, the role of endogenous anti-inflammatory pathways in atheroma has received much less attention. Therefore, using cDNA microarrays, we screened for genes regulated by prostaglandin E 2 (PGE 2 ), a potential endogenous anti-inflammatory mediator, in lipopolysaccharide (LPS)-treated human macrophages (M⌽). PGE 2 (50 nM) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1␣ and -1␤, and interferon-inducible protein-10. PGE 2 also inhibited the tumor necrosis factor-␣-, interferon-␥-, and interleukin-1␤-mediated expression of these chemokines. In contrast to the case of M⌽, PGE 2 did not suppress chemokine expression in human endothelial and smooth muscle cells (SMC) treated with LPS and pro-inflammatory cytokines. To assess the potential paracrine effect of endogenous PGE 2 on macrophagederived chemokine production, we co-cultured M⌽ with SMC in the presence of LPS. In these co-cultures, cyclooxygenase-2-dependent PGE 2 production exceeded that in the mono-cultures, and MIP-1␤ declined significantly compared with M⌽ cultured without SMC. We further documented prominent expression of the PGE 2 receptor EP4 in M⌽ in both culture and human atheroma. Moreover, a selective EP4 antagonist completely reversed PGE 2 -mediated suppression of chemokine production. Thus, endogenous PGE 2 may modulate inflammation during atherogenesis and other inflammatory diseases by suppressing macrophage-derived chemokine production via the EP4 receptor.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Takayama¹,

García‐Cardeña

Sukhova³

et al. 2002

Journal of Biological Chemistry

306

272

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“…Chemokine production from inflammatory cells has been well documented, but we and others have also shown in in vitro studies that smooth muscle cells can be potent sources of chemokines, including IL-8, MCP-1, RANTES, and MIP-1␣, when stimulated with proinflammatory cytokines. 36,52,53 These chemokines can also be produced by stimulated endothelial cells. 34,37,41,54,55 We have shown that cultured human VSMCs constitutively express mRNA for the chemokine receptors CCR-1 and CCR-2.…”

Section: Discussionmentioning

confidence: 99%

Human Vascular Smooth Muscle Cells Express Receptors for CC Chemokines

Hayes

Jordan

Towers

et al. 1998

ATVB

135

101

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“…It has been shown that MCP-1 is expressed in vitro by various cells such as macrophages, endothelial cells, and smooth muscle cells in response to various proinflammatory stimuli Wang et al, 1991). MCP-1 expression has been shown also in vivo such as within the atherosclerotic lesions of blood vessels from man, rabbits and hypercholesterolaemic primates or within synovial tissues from patients with rheumatoid arthritis (Nelken et al, 1991;Yla-Huttuala et al, 1991;Koch et al, 1992;Villiger et al, 1992;Yu et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

The effect of a synthetic 7‐thiaprostaglandin E₁ derivative, TEI‐6122, on monocyte chemoattractant protein‐1 induced chemotaxis in THP‐1 cells

Tanaka

Minoshima

Endo

1995

British J Pharmacology

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1 The ability of various prostaglandins (PGs) to inhibit monocyte chemotaxis induced by monocyte chemoattractant protein-i (MCP-1) was investigated with a human monocytic leukaemia cell line, THP-1. Moreover, to investigate the mechanism of the inhibitory action of PGs the involvement of either intracellular adenosine 3': 5'-cyclic monosphosphate (cyclic AMP) accumulation or intracellular Ca2+ mobilization was studied.2 TEI-6122, a synthetic 7-thia-PGE, derivative, inhibited chemotaxis of THP-1 cells induced by MCP-1 with an IC50 of 1.5 pM. Its inhibitory activity was 1000 fold more than that of PGE1 and PGE2 (IC50=2.8 nM and 0.9 nM, respectively), which were more potent than other PGs such as PGAI, PGA2, 4 TEI-6122 and PGE1 (4 gM) transiently increased intracellular calcium levels in THP-1 cells. When added prior to MCP-1, both PGs partially suppressed the increased in Ca2+ caused by this cytokine.There were no significant differences between the activity of TEI-6122 and PGEI in either respect. 5 It is concluded that TEI-6122, a synthetic 7-thia-PGE, derivative is a much more potent inhibitor of MCP-1-induced THP-1 cell chemotaxis than PGEI and PGE2 which are the best inhibitors among the natural PGs tested, while neither intracellular cyclic AMP accumulation nor effects on Ca2+ mobilization account for the extremely potent inhibitory activity of TEI-6122. Thus, either a novel PGE2 receptor (EP receptor) or a novel intracellular signal transduction system may be involved in the extremely potent chemotaxis inhibitory activity of TEI-6122.

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Expression of monocyte chemotactic protein and interleukin-8 by cytokine-activated human vascular smooth muscle cells.

Abstract: The present study was designed to investigate the capacity of human vascular smooth muscle cells (SMCs) to produce a cytokine chemotactic for monocytes (monocyte chemotactic protein

Cited by 172 publications

References 38 publications

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Human Vascular Smooth Muscle Cells Express Receptors for CC Chemokines

The effect of a synthetic 7‐thiaprostaglandin E₁ derivative, TEI‐6122, on monocyte chemoattractant protein‐1 induced chemotaxis in THP‐1 cells

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Expression of monocyte chemotactic protein and interleukin-8 by cytokine-activated human vascular smooth muscle cells.

Abstract: The present study was designed to investigate the capacity of human vascular smooth muscle cells (SMCs) to produce a cytokine chemotactic for monocytes (monocyte chemotactic protein

Cited by 172 publications

References 38 publications

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Human Vascular Smooth Muscle Cells Express Receptors for CC Chemokines

The effect of a synthetic 7‐thiaprostaglandin E1 derivative, TEI‐6122, on monocyte chemoattractant protein‐1 induced chemotaxis in THP‐1 cells

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The effect of a synthetic 7‐thiaprostaglandin E₁ derivative, TEI‐6122, on monocyte chemoattractant protein‐1 induced chemotaxis in THP‐1 cells