Thromboxane, prostacyclin and isoprostanes: therapeutic targets in atherogenesis

Dogné, Jean‐Michel; Hanson, Julien; Praticò, Domenico

doi:10.1016/j.tips.2005.10.001

Cited by 89 publications

(71 citation statements)

References 65 publications

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“…PGI 2 is an antithrombotic and vasodilator molecule that can decrease vascular remodeling and cholesterol uptake (51,52). This is particularly evident from the fact that disruption of the prostacyclin receptor gene leads to increased intimamedium ratio in response to vascular injury and promotes initiation and progression of atherosclerosis in hyperlipidemic mouse (53,54), suggesting a protective role for prostacyclin in vascular remodeling.…”

Section: Figurementioning

confidence: 99%

“…This is particularly evident from the fact that disruption of the prostacyclin receptor gene leads to increased intimamedium ratio in response to vascular injury and promotes initiation and progression of atherosclerosis in hyperlipidemic mouse (53,54), suggesting a protective role for prostacyclin in vascular remodeling. TXA 2 , in contrast, is a prothrombotic and vasoconstricting agent, and enhances vascular remodeling (51,52). Because PGI 2 and TXA 2 exert opposing influences in the cardiovascular system, the up-regulation of the expression of COX-2, PGE 2 synthase, and PGI 2 synthase in HCAEC by histamine emphasizes its importance in the maintenance of vascular integrity.…”

Section: Figurementioning

confidence: 99%

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Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

Tan

Essengue

Talreja

et al. 2007

The Journal of Immunology

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Although histamine plays an essential role in inflammation, its influence on cyclooxygenases (COX) and prostanoid homeostasis is not well understood. In this study, we investigated the effects of histamine on the expression of COX-1 and COX-2 and determined their contribution to the production of PGE2, prostacyclin (PGI2), and thromboxane A2 in human coronary artery endothelial cells (HCAEC). Incubation of HCAEC monolayers with histamine resulted in marked increases in the expression of COX-2 and production of PGI2 and PGE2 with no significant change in the expression of COX-1. Histamine-induced increases in PGI2 and PGE2 production were due to increased expression and function of COX-2 because gene silencing by small interfering RNA or inhibition of the catalytic activity by a COX-2 inhibitor blocked prostanoid production. The effects of histamine on COX-2 expression and prostanoid production were mediated through H1 receptors. In addition to the direct effect, histamine was found to amplify LPS-stimulated COX-2 expression and PGE2 and PGI2 production. In contrast, histamine did not stimulate thromboxane A2 production in resting or LPS-activated HCAEC. Histamine-induced increases in the production of PGE2 and PGI2 were associated with increased expression of mRNA encoding PGE2 and PGI2 synthases. The physiological role of histamine on the regulation of COX-2 expression in the vasculature is indicated by the findings that the expression of COX-2 mRNA, but not COX-1 mRNA, was markedly reduced in the aortic tissues of histidine decarboxylase null mice. Thus, histamine plays an important role in the regulation of COX-2 expression and prostanoid homeostasis in vascular endothelium.

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Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

Tan

Essengue

Talreja

et al. 2007

The Journal of Immunology

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“…Up-regulation of serum and plasma CD40L, urinary isoprostanes, and P-selectin are thought to represent the initiation of the atherothrombotic cascade by stimulating cytokines (such as tumor necrosis factor-α, whose effects are mediated in part by TNFR2) in response to damage of the endothelium or vascular smooth muscle. 19,20 P-selectin and ICAM-1 are involved in the rolling phase of leukocyte adhesion and early plaque development. 15,19 MCP-1, a chemokine found in atherosclerotic plaque, attracts monocytes to developing plaque.…”

Section: Introductionmentioning

confidence: 99%

“…19,20 P-selectin and ICAM-1 are involved in the rolling phase of leukocyte adhesion and early plaque development. 15,19 MCP-1, a chemokine found in atherosclerotic plaque, attracts monocytes to developing plaque. 21,22 MPO, a leukocyte enzyme, is elevated in culprit lesions of patients with acute coronary syndrome.…”

Section: Introductionmentioning

confidence: 99%

Relation of smoking status to a panel of inflammatory markers: The Framingham offspring

et al. 2008

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Aims-We sought to investigate the hypothesis that smoking is accompanied by systemic inflammation.Methods and Results-We examined the relation of smoking to 11 systemic inflammatory markers in Framingham Study participants (n=2944, mean age 60 years, 55% women, 12% ethnic minorities) examined from 1998-2001. The cohort was divided into never (n=1149), former (n=1424), and current smokers with last cigarette >6 hours (n=134) or ≤6 hours (n=237) prior to phlebotomy. In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p<0.0045 to account for multiple testing) for every inflammatory marker tested, except for serum CD40 ligand (CD40L), myeloperoxidase (MPO) and tumor necrosis factor receptor-2 (TNFR2). With multivariable-adjustment, pair-wise comparisons with never smokers revealed that former smokers had significantly lower concentrations of plasma CD40L (p<0.0001) and higher concentrations of C-reactive protein (p=0.002).Conclusions-As opposed to never smokers, those with acute cigarette smoke exposure (≤6 hours) had significantly higher concentrations of all markers (p<0.0001) except serum CD40L, MPO, and TNFR2; plasma CD40L were significantly lower. Compared with never smokers, cigarette smokers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state.

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“…트롬복산 수용체는 인간에서는 TPα과 TPβ, 두 가지 isoform을 가지고 있으며 이들의 활성이 죽상동맥경화증과 같은 혈관성 염증질환에 관여한다 [15,16]. 그리고 트롬복산 수용체의 발현 및 트롬복산 수용체의 리간드의 혈장 농도가 여러 가지 심혈관계 질환에서 증가되어 있다고 보고되고 있 다 [17,18].…”

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Activation of Thromboxane Receptor Mediates Interleukin-8 Expression in Endothelial Cells

Jeon¹,

Kim²,

Park³

et al. 2013

KSBB Journal

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Thromboxane A 2 (TXA 2 ) is one of major proinflammatory mediators, plays an important role in the development of vascular inflammatory diseases. TXA 2 acting through the thromboxane receptor regulates multiple pathways and genes in a variety of cells. In this study, we report that the activation of thromboxane receptor with U46619 increases the interleukin-8 (IL-8) mRNA in vascular endothelial cells. We also demonstrated that U46619 produces the activations of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK), which is required for endothelial IL-8 production. And U46619 enhanced mRNA stability of IL-8 transcripts in endothelial cells. Moreover, inhibition of ERK1/2 or p38MAPK reduced monocyte adhesion to aortic endothelium stimulated by U46619. Therefore, these results suggest that activation of thromboxane receptor promotes the expression of IL-8 via ERK1/2 and p38MAPK activation in endothelial cells.

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Thromboxane, prostacyclin and isoprostanes: therapeutic targets in atherogenesis

Cited by 89 publications

References 65 publications

Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

Histamine Directly and Synergistically with Lipopolysaccharide Stimulates Cyclooxygenase-2 Expression and Prostaglandin I2 and E2 Production in Human Coronary Artery Endothelial Cells

Relation of smoking status to a panel of inflammatory markers: The Framingham offspring

Activation of Thromboxane Receptor Mediates Interleukin-8 Expression in Endothelial Cells

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