Dexamethasone and Enalapril Suppress Intimal Hyperplasia Individually but Have No Synergistic Effect

Petrik, Pavel V.; Law, Michael M.; Moore, Wesley S.; Colburn, Michael D.; Quiñones-Baldrich, William J.; Gelabert, Hugh A.

doi:10.1007/s100169900143

Cited by 12 publications

(11 citation statements)

References 19 publications

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“…Multiple agents have been examined including antihypertensives, antilipid, antiplatelet, and anti-inflammatory agents [11,[22][23][24][25]. This laboratory has recently shown that treatment with the glucocorticoid dexamethasone significantly reduces intimal hyperplasia following balloon in- jury of the rat carotid artery [11].…”

Section: Discussionmentioning

confidence: 99%

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Dexamethasone Suppresses Vascular Smooth Muscle Cell Proliferation

Reil¹,

Sarkar²,

Kashyap³

et al. 1999

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

“…Recent work in our laboratory has demonstrated that treatment with dexamethasone leads to a marked decrease in the development of hyperplasia in a rodent model of intimal hyperplasia [11]. The mechanisms behind this inhibition are unknown.…”

Section: Introductionmentioning

confidence: 97%

Dexamethasone Suppresses Vascular Smooth Muscle Cell Proliferation

Reil¹,

Sarkar²,

Kashyap³

et al. 1999

Journal of Surgical Research

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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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“…We chose dexamethasone (DEX), an immune suppressant, as the model drug, because it has been shown to reduce the development of intimal hyperplasia (Petrik et al, 1998) and exhibit both anti-inflammation effects on ECs and anti-migration and anti-proliferation effects on SMCs (Park and Yoo, 2006; Van Put et al, 1995). Cellular uptake of the control and GPIb-conjugated NPs was detected in human aortic endothelial cells (HAECs) by fluorescent measurements and confocal microscopy imaging.…”

Section: Introductionmentioning

confidence: 99%

Biodegradable nanoparticles mimicking platelet binding as a targeted and controlled drug delivery system

Kona

Dong

Liu

et al. 2012

International Journal of Pharmaceutics

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This research aims to develop targeted nanoparticles as drug carriers to the injured arterial wall under fluid shear stress by mimicking the natural binding ability of platelets via interactions of glycoprotein Ib-alpha (GP Ibα) of platelets with P-selectin of damaged endothelial cells (ECs) and/or with von Willebrand factor (vWF) of the subendothelium. Drug-loaded poly (D, L-lactic-co-glycolic acid) (PLGA) nanoparticles were formulated using a standard emulsion method and conjugated with glycocalicin, the external fraction of platelet GPIbα, via carbodiimide chemistry. Surface-coated and cellular uptake studies in ECs showed that conjugation of PLGA nanoparticles with GPIb significantly increased nanoparticle adhesion to P-selectin- and vWF-coated surfaces as well as nanoparticle uptake by activated ECs under fluid shear stresses. In addition, effects of nanoparticle size and shear stress on adhesion efficiency were characterized through parallel flow chamber studies. The observed decrease in bound nanoparticle density with increased particle sizes and shear stresses is also explained through a computational model. Our results demonstrate that the GPIb-conjugated PLGA nanoparticles can be used as a targeted and controlled drug delivery system under flow conditions at the site of vascular injury.

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Dexamethasone and Enalapril Suppress Intimal Hyperplasia Individually but Have No Synergistic Effect

Cited by 12 publications

References 19 publications

Dexamethasone Suppresses Vascular Smooth Muscle Cell Proliferation

Dexamethasone Suppresses Vascular Smooth Muscle Cell Proliferation

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

Biodegradable nanoparticles mimicking platelet binding as a targeted and controlled drug delivery system

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