In VivoRole of Glucocorticoids in Barotrauma Vascular Repair and Fibrosis

Karim, M.Asad; Frizzell, Scott; Inman, Lindsey; Shinn, Marlene; Miller, D. Douglas

doi:10.1006/jmcc.1996.0330

Cited by 10 publications

(7 citation statements)

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“…Further, the systemic effects of glucocorticoids on cardiovascular risk factors (glucose, insulin, lipids and blood pressure) may offset beneficial effects within the vessel wall. Dexamethasone reduces cholesterol ester accumulation in the aorta [133], and glucocorticoids (dexamethasone, hydrocortisone) inhibit neointimal lesion formation in rats [134,135], rabbits [136][137][138] and dogs [139] (with a few contradictory reports [140,141]). Clinical trials in humans, by contrast, have proved disappointing (with notable exceptions [130]): methylprednisolone did not inhibit restenosis after coronary angioplasty [142] or stent implantation [143], whilst the combination of a glucocor-570 P. W. F. Hadoke et al Intra-vascular glucocorticoid metabolism ticoid with colchicine increased the risk of coronary aneurysm following stent placement [144].…”

Section: Neointimal Proliferationmentioning

confidence: 99%

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

Hadoke

Macdonald

Logie

et al. 2006

Cell. Mol. Life Sci.

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The ability of glucocorticoids to directly alter arterial function, structure and the inflammatory response to vascular injury may contribute to their well-established link with the development of cardiovascular disease. Recent studies have emphasised the importance of tissue-specific regulation of glucocorticoid availability by the 11 beta-hydroxysteroid dehydrogenase (11HSD) isozymes, which inter-convert active glucocorticoids and their inactive metabolites. The expression of both type 1 and type 2 11HSDs in the arterial wall suggests that prereceptor metabolism of glucocorticoids may have a direct impact on vascular physiology. Indeed there is evidence that 11HSDs influence glucocorticoid-mediated changes in vascular contractility, vascular structure, the inflammatory response to injury and the growth of new blood vessels. Hence, inhibition of 11HSD isozymes may provide a novel therapeutic target in vascular disease.

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Section: Neointimal Proliferationmentioning

confidence: 99%

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

Hadoke

Macdonald

Logie

et al. 2006

Cell. Mol. Life Sci.

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“…, 2006). Not all studies in animals have yielded positive results, however, as dexamethasone treatment did not reduce neointimal hyperplasia after angioplasty in the rabbit (Karim et al. , 1997) or in the pig (Lincoff et al.…”

Section: Glucocorticoids and Cardiovascular Pathophysiologymentioning

confidence: 99%

“…This approach may also have potential in the prevention of chronic graft disease as short-term (7 days) oral dexamethasone (0.15 mg -1 ·kg -1 ·day -1 ) reduced vein graft thickening in ApoE3leiden mice (Schepers et al, 2006). Not all studies in animals have yielded positive results, however, as dexamethasone treatment did not reduce neointimal hyperplasia after angioplasty in the rabbit (Karim et al, 1997) or in the pig (Lincoff et al, 1997). Initial clinical trials were also disappointing: methylprednisolone did not inhibit restenosis after coronary angioplasty (Pepine et al, 1990) or stenting (Reimers et al, 1998) while dexamethasone-drug eluting stents (D-DES) have not reduced the incidence of restenosis (Hoffmann et al, 2004a;Ribichini et al, 2007b).…”

Section: Social Stressmentioning

confidence: 99%

Therapeutic manipulation of glucocorticoid metabolism in cardiovascular disease

Hadoke

Iqbal

Walker

2009

British J Pharmacology

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The therapeutic potential for manipulation of glucocorticoid metabolism in cardiovascular disease was revolutionized by the recognition that access of glucocorticoids to their receptors is regulated in a tissue-specific manner by the isozymes of 11b-hydroxysteroid dehydrogenase. Selective inhibitors of 11b-hydroxysteroid dehydrogenase type 1 have been shown recently to ameliorate cardiovascular risk factors and inhibit the development of atherosclerosis. This article addresses the possibility that inhibition of 11b-hydroxsteroid dehydrogenase type 1 activity in cells of the cardiovascular system contributes to this beneficial action. The link between glucocorticoids and cardiovascular disease is complex as glucocorticoid excess is linked with increased cardiovascular events but glucocorticoid administration can reduce atherogenesis and restenosis in animal models. There is considerable evidence that glucocorticoids can interact directly with cells of the cardiovascular system to alter their function and structure and the inflammatory response to injury. These actions may be regulated by glucocorticoid and/or mineralocorticoid receptors but are also dependent on the 11b-hydroxysteroid dehydrogenases which may be expressed in cardiac, vascular (endothelial, smooth muscle) and inflammatory (macrophages, neutrophils) cells. The activity of 11b-hydroxysteroid dehydrogenases in these cells is dependent upon differentiation state, the action of pro-inflammaotory cytokines and the influence of endogenous inhibitors (oxysterols, bile acids). Further investigations are required to clarify the link between glucocorticoid excess and cardiovascular events and to determine the mechanism through which glucocorticoid treatment inhibits atherosclerosis/restenosis. This will provide greater insights into the potential benefit of selective 11b-hydroxysteroid dehydrogenase inhibitors in treatment of cardiovascular disease.

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“…High lung inflation increases wall stress in rabbit pulmonary capillaries, causes an increase in expression of procollagen III mRNA, basic fibroblast growth factor, and transforming growth factor b1(TGFb1) [19]. Balloon angioplasty of rabbit atherogenic vessels increased the gene expression of procollagens I and III, and TGFb, and there were direct correlations between TGFb1 and both Type I and Type III procollagen mRNA expressions [20]. Once translation of the mRNAs encoding the pre-procollagens has taken place, intracellular post-translational modifications result in the formation of soluble triplehelical procollagen molecules, the precursors of the fibrillar collagens [4].…”

Section: 34mentioning

confidence: 99%