Dexamethasone inhibits macrophage accumulation after balloon arterial injury in cholesterol fed rabbits

Poon, Michael; Gertz, S. David; Fallon, John T.; Wiegman, Pete; Berman, Joan W.; Sarembock, Ian J.; Taubman, Mark B.

doi:10.1016/s0021-9150(00)00605-5

Cited by 55 publications

(42 citation statements)

References 57 publications

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“…Glucocorticoid treatment has been shown to reduce macrophage accumulation in a model of cholesterolinduced atherosclerosis (Poon et al 2001) and decrease neointimal proliferation following balloon angioplasty (Villa et al 1994). A role for macrophage GR signalling in a model of atherosclerosis has recently been identified by transplanting bone marrow derived from macrophage GR-null mice into LDL receptor deficient mice (Preusch et al 2008).…”

Section: Atherosclerosis and Macrophage Grmentioning

confidence: 99%

Corticosteroid receptors, macrophages and cardiovascular disease

Rickard¹,

Young²

2009

Journal of Molecular Endocrinology

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The mineralocorticoid receptor (MR) and glucocorticoid receptor are ligand-activated transcription factors that have important physiological and pathophysiological actions in a broad range of cell types including monocytes and macrophages. While the glucocorticoids cortisol and corticosterone have well-described anti-inflammatory actions on both recruited and tissue resident macrophages, a role for the mineralocorticoid aldosterone in these cells is largely undefined. Emerging evidence, however, suggests that MR signalling may promote pro-inflammatory effects. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on diseases involving inflammation, with a particular focus on cardiovascular disease.

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Section: Atherosclerosis and Macrophage Grmentioning

confidence: 99%

Corticosteroid receptors, macrophages and cardiovascular disease

Rickard¹,

Young²

2009

Journal of Molecular Endocrinology

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“…5 Experimental studies using animal models of hyperlipidemia-induced atherosclerosis have demonstrated a beneficial role of GC in cholesterol-induced atherosclerosis as well as in postangioplasty restenosis models. 6,7 However, next to their ability to decrease atherosclerosis and restenosis, GCs are also known to exert the risk of atherogenesis, depending on the experimental or clinical conditions. 8 Although exogenous GCs are known to promote osteoporosis, 9 physiological concentrations of GCs can exert an anabolic effect on bone formation.…”

Section: See Accompanying Article On Page 2096mentioning

confidence: 99%

Critical Role of Macrophages in Glucocorticoid Driven Vascular Calcification in a Mouse-Model of Atherosclerosis

Preusch

Rattazzi

Albrecht

et al. 2008

ATVB

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Objective-Macrophage-derived products are known to play a crucial role during atherogenesis and vascular calcification.Glucocorticoids (GC) are important modulators of immune cell functions, but their specific effects on macrophages behavior during plaque formation are not defined. The present study was therefore designed to investigate the effects of macrophage-specific deletion of the glucocorticoid receptor (GR LysMCre ) on atherogenesis and vascular calcification in a hyperlipidemic mouse-model. Methods and Results-Bone marrow was isolated from GRLysMCre mice and wild-type controls (GR flox ) and subsequently transplanted into lethally irradiated LDL-receptor-deficient mice. Animals were fed a Western-type diet for 15 or 24 weeks, and atherosclerotic lesions within the aortic sinus were evaluated. At both time points, no significant difference in serum lipid and corticosterone concentrations, atherosclerotic lesion size and macrophage-content within the lesions could be observed. However, GR LysMCre mice showed less calcification as well as a significant reduction of RANKL, BMP2, and Msx2 expression within the vasculature. In vitro studies using conditioned media from macrophages which had been stimulated with dexamethasone demonstrated a dose-dependent increase in calcium deposition by vascular smooth muscle cells. Conclusion-This

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“…GCs are potent inhibitors of MCP-1 synthesis in a variety of cell types (21,32,36,54), including SMCs (44)(45)(46)(47). GCs are reported to suppress intimal hyperplasia (6,55) and atherosclerosis (3,43).…”

mentioning

confidence: 99%

“…We have previously reported that the GC dexamethasone (Dex) markedly reduces the accumulation of MCP-1 mRNA in SMCs and that the effect is almost exclusively due to changes in mRNA stability (a reduction in the half-life [t 1/2 ] of MCP-1 mRNA from Ͼ3 h to Ͻ15 min) (43,45,46). We have also demonstrated that this effect is mediated by the glucocorticoid receptor (GR) and involves an apparently novel mechanism in which the GR binds directly to MCP-1 mRNA and facilitates its degradation (11).…”

mentioning

confidence: 99%

Y-Box Binding Protein 1 and RNase UK114 Mediate Monocyte Chemoattractant Protein 1 mRNA Stability in Vascular Smooth Muscle Cells

Dhawan

Liu

Pytlak

et al. 2012

Molecular and Cellular Biology

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Monocyte chemoattractant protein 1 (MCP-1) plays a pivotal role in many inflammatory processes, including the progression of atherosclerosis and the response of the arterial wall to injury. We previously demonstrated that dexamethasone (Dex) inhibits MCP-1 mRNA accumulation in smooth muscle cells by decreasing its half-life. The effect of Dex was dependent upon the glucocorticoid receptor (GR) and independent of new transcription. Using RNA affinity and column chromatography, we have identified two proteins involved in regulating MCP-1 mRNA stability: Y-box binding protein 1 (YB-1), a multifunctional DNA/RNA-binding protein, and endoribonuclease UK114 (UK). By immunoprecipitation, YB and GR formed a complex present in equal amounts in extracts from untreated and Dex-treated cells. YB-1, UK, and GR small interfering RNA (siRNA) substantially inhibited the effect of Dex on MCP-1 mRNA accumulation. In addition, YB-1 antibody blocked the degradation of MCP-1 mRNA by cytoplasmic extracts from the Dex-treated cells. The degradative activity of extracts immunoprecipitated with antibodies to either YB-1 or GR was blocked with UK antibody. UK did not degrade MCP-1 mRNA; however, upon addition to nondegrading control extracts, it rapidly degraded MCP-1 mRNA. These studies define new roles for GR, YB-1, and UK in the formation of a molecular complex that degrades MCP-1 mRNA.

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Dexamethasone inhibits macrophage accumulation after balloon arterial injury in cholesterol fed rabbits

Cited by 55 publications

References 57 publications

Corticosteroid receptors, macrophages and cardiovascular disease

Corticosteroid receptors, macrophages and cardiovascular disease

Critical Role of Macrophages in Glucocorticoid Driven Vascular Calcification in a Mouse-Model of Atherosclerosis

Y-Box Binding Protein 1 and RNase UK114 Mediate Monocyte Chemoattractant Protein 1 mRNA Stability in Vascular Smooth Muscle Cells

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