Local Delivery of Ethanol Inhibits Intimal Hyperplasia in Pig Coronary Arteries After Balloon Injury

Liu, Ming Wei; Anderson, Peter G.; Luo, Jian F.; Roubin, Gary S.

doi:10.1161/01.cir.96.7.2295

Cited by 30 publications

(22 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…21 Considerable reductions in neointimal hyperplasia, including SMC proliferation, were also observed in pigs after angioplasty. 20 Interestingly, in the last model, local delivery of 15% ethanol in the immediate postinjury phase was effective in reducing the size of neointimal lesions, which suggests that early signaling events might be specifically targeted by ethanol. Ethanol-induced inhibition of rat vascular SMC proliferation and activation of p42/p44 MAPK in vitro was subsequently demonstrated.…”

Section: Discussionmentioning

confidence: 91%

See 1 more Smart Citation

Ethanol Inhibits Fibroblast Growth Factor–Induced Proliferation of Aortic Smooth Muscle Cells

Ghiselli

Chen

Kaou

et al. 2003

ATVB

View full text Add to dashboard Cite

Objective-Epidemiological studies have demonstrated that moderate alcohol consumption reduces mortality associated with coronary artery disease. The protective effect is correlated with the amount of ethanol consumed but is unrelated to the form of alcoholic beverage. Adoption of a favorable lipoprotein profile accounts for about half of the protective action of alcohol, but the remaining causative factors remain conjectural. Fibroblast growth factors (FGFs) play important roles in mediating smooth muscle cell (SMC) proliferation and migration, which are key factors in the atherosclerotic process. In the present study, we examined the effect of ethanol on FGF-mediated SMC growth and signaling. Methods and Results-Pharmacologically relevant concentrations of ethanol inhibited the proliferation of a rat aortic SMC line (SV40LT-SMCs) in response to FGF1 and FGF2. Human aortic SMC growth was similarly inhibited by ethanol. Transition into the G 2 /M phase was specifically affected. FGF-mediated phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK) c-Raf, MAP kinase kinase kinase, MEK1/2 MAP kinase, kinase, stress-activated protein kinase/c-Jun-NH 2 -terminal kinase, and p38 MAPK were variably reduced by ethanol. The inhibition of intracellular signaling by ethanol was correlated with inhibition of FGF receptor autophosphorylation. By contrast, neither epidermal growth factor receptor autophosphorylation nor epidermal growth factor-mediated p42/p44 MAPK activation was affected by ethanol. Conclusions-The

show abstract

Section: Discussionmentioning

confidence: 91%

“…Hendrickson et al 19 reported that ethanol inhibits mitogen-activated protein kinase (MAPK) activity and the growth of SMCs in vitro. Ethanol also inhibits intimal hyperplasia in the arteries of pigs 20 and rabbits 21 after angioplasty.…”

mentioning

confidence: 96%

Ethanol Inhibits Fibroblast Growth Factor–Induced Proliferation of Aortic Smooth Muscle Cells

Ghiselli

Chen

Kaou

et al. 2003

ATVB

View full text Add to dashboard Cite

show abstract

“…21 After anesthesia induction and intubation, heparin (200 U/kg) and bretylium (50 mg) were given as an intravenous bolus, and 10 mg of nifedipine was given sublingually. Via a right femoral artery approach, a balloon catheter, 20 mm long with a diameter 20% larger than the arterial diameter, was used to perform the dilation injury.…”

Section: Balloon Angioplasty Procedures For Swine Coronary Restenosismentioning

confidence: 99%

Cyclic GMP–Dependent Protein Kinase Expression in Coronary Arterial Smooth Muscle in Response to Balloon Catheter Injury

Anderson

Boerth

Liu

et al. 2000

ATVB

Self Cite

View full text Add to dashboard Cite

Abstract-Arterial smooth muscle cells undergo phenotypic and proliferative changes in response to balloon catheter injury. Nitric oxide (NO) and cGMP have been implicated in the inhibition of vascular smooth muscle cell proliferation and phenotypic modulation in cultured-cell studies. We have examined the expression of the major cGMP receptor protein in smooth muscle, cGMP-dependent protein kinase I (PKG), in response to balloon catheter injury in the swine coronary artery. On injury, there was a transient decrease in the expression of PKG in neointimal smooth muscle cells when compared with medial smooth muscle cells. The decrease in PKG expression was observed in the population of proliferating cells expressing the extracellular matrix protein osteopontin but not in cells present in the uninjured portion of the media. Coincident with the suppression of PKG expression in neointimal cells after injury, there was a marked increase in the expression of type II NO synthase (inducible NOS [iNOS], NOS-II) in the neointimal cells. These results suggest that PKG expression is transiently reduced in response to injury in the population of coronary arterial smooth muscle cells that are actively proliferating and producing extracellular matrix proteins. The reduction in PKG expression is also correlated temporally with increases in inflammatory activity in the injured vessels as assessed by iNOS expression. Coupled with our current knowledge regarding the role of PKG in the regulation of cultured cell phenotypes, these results imply that PKG may also regulate phenotypic modulation of vascular smooth muscle cells in vivo as well.

show abstract

“…1,2 Early local administration of numerous therapeutic agents into injured vessel walls poorly inhibited smooth muscle cell proliferation. [3][4][5][6][7][8][9][10][11][12] Recently, newer stent-based drug-delivery systems, particularly devices incorporating hydrophobic antiproliferative agents, have been successful in the clinic. [13][14][15] These promising results indicate that local deposition and prolonged release of appropriate antiproliferative agents can effectively ameliorate restenosis.…”

mentioning

confidence: 99%

Targeted Antiproliferative Drug Delivery to Vascular Smooth Muscle Cells With a Magnetic Resonance Imaging Nanoparticle Contrast Agent

et al. 2002

View full text Add to dashboard Cite

Background-Restenosis is a serious complication of coronary angioplasty that involves the proliferation and migration of vascular smooth muscle cells (VSMCs) from the media to the intima, synthesis of extracellular matrix, and remodeling. We have previously demonstrated that tissue factor-targeted nanoparticles can penetrate and bind stretch-activated vascular smooth muscles in the media after balloon injury. In the present study, the concept of VSMC-targeted nanoparticles as a drug-delivery platform for the prevention of restenosis after angioplasty is studied. Methods and Results-Tissue factor-targeted nanoparticles containing doxorubicin or paclitaxel at 0, 0.2, or 2.0 mole% of the outer lipid layer were targeted for 30 minutes to VSMCs and significantly inhibited their proliferation in culture over the next 3 days. Targeting of the nanoparticles to VSMC surface epitopes significantly increased nanoparticle antiproliferative effectiveness, particularly for paclitaxel. In vitro dissolution studies revealed that nanoparticle drug release persisted over one week. Targeted antiproliferative results were dependent on the hydrophobic nature of the drug and noncovalent interactions with other surfactant components. Molecular imaging of nanoparticles adherent to the VSMC was demonstrated with high-resolution T 1 -weighted MRI at 4.7T. MRI 19 F spectroscopy of the nanoparticle core provided a quantifiable approach for noninvasive dosimetry of targeted drug payloads. Conclusions-These data suggest that targeted paramagnetic nanoparticles may provide a novel, MRI-visualizable, and quantifiable drug delivery system for the prevention of restenosis after angioplasty.

show abstract

Local Delivery of Ethanol Inhibits Intimal Hyperplasia in Pig Coronary Arteries After Balloon Injury

Abstract: Local delivery of 15% ethanol solution to pig coronary arteries significantly decreased the SMC proliferative activity and neointimal formation induced by balloon dilation injury.

Cited by 30 publications

References 34 publications

Ethanol Inhibits Fibroblast Growth Factor–Induced Proliferation of Aortic Smooth Muscle Cells

Ethanol Inhibits Fibroblast Growth Factor–Induced Proliferation of Aortic Smooth Muscle Cells

Cyclic GMP–Dependent Protein Kinase Expression in Coronary Arterial Smooth Muscle in Response to Balloon Catheter Injury

Targeted Antiproliferative Drug Delivery to Vascular Smooth Muscle Cells With a Magnetic Resonance Imaging Nanoparticle Contrast Agent

Contact Info

Product

Resources

About