Effects of a single local administration of cilostazol on neointimal formation in balloon-injured rat carotid artery

Ishizaka, Nobukazu; Taguchi, Junichi; Kimura, Yukio; Ikari, Yuji; Aizawa, Toru; Togo, Masami; Miki, Keizaburoh; Kurokawa, Kiyoshi; Ohno, Minoru

doi:10.1016/s0021-9150(98)00147-6

Cited by 82 publications

(56 citation statements)

References 22 publications

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“…Moreover, cilostazol has a direct effect on the proliferation of SMC, as it inhibited cell cycle progression of VSMC through up-regulation of anti-oncogenes, p53-p21 [6]. Consistent with previous reports [8], we showed that cilostazol inhibited neointimal formation after balloon injury in a non-diabetic rat model. A single model however, might be far from the clinical situation.…”

Section: Discussionsupporting

confidence: 92%

“…It increases of the concentration of cyclic AMP (cAMP) by selectively blocking PDE3, resulting in the inhibition of platelet aggregation. As cilostazol is also known to suppress the growth of VSMC in vitro [5±7] and in vivo [8], some investigators have examined whether cilostazol can prevent restenosis in clinical situations. Despite the small number of patients, several groups have reported the inhibition of restenosis by cilostazol [9±15].…”

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confidence: 99%

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Inhibition of neointimal formation after balloon injury by cilostazol, accompanied by improvement of endothelial dysfunction and induction of hepatocyte growth factor in rat diabetes model

et al. 2001

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Inhibition of neointimal formation after balloon injury by cilostazol, accompanied by improvement of endothelial dysfunction and induction of hepatocyte growth factor in rat diabetes model

et al. 2001

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“…Accordingly, enhanced apoptosis of the neointimal SMCs is likely to be involved in the mechanisms of prevention of neointima formation by Y27632. It is noteworthy that Y27632 enhanced SMC apoptosis in the injured artery without any effect on cell replication; in contrast, SMC replication is prevented by most other inhibitors of neointima formation, including endothelin receptor antagonist, 19 cilostazol, 20 and tranilast. 21 The precise molecular mechanisms whereby Y27632 enhanced neointimal SMC apoptosis remain to be determined.…”

Section: Discussionmentioning

confidence: 96%

Role of Rho-Associated Kinase in Neointima Formation After Vascular Injury

et al. 2001

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Background —The Rho/Rho-associated kinase (Rho-kinase) system is implicated in various cellular functions, including migration, proliferation, and apoptosis. Because a possible role of the system is suggested in neointima formation after vascular injury, we sought to examine whether a new specific Rho-kinase inhibitor, Y27632, prevents neointima formation of the balloon-injured rat carotid artery, and if so, to investigate the effects of Y27632 on migration, proliferation, and apoptosis of smooth muscle cells (SMCs) in the injured artery. Methods and Results —Y27632 was administered intraperitoneally from 1 day before to 14 days after vascular injury. Treatment with Y27632 inhibited phenylephrine-induced Rho-kinase activation in the carotid artery on the basis of immunoblotting against the phosphorylated myosin-binding subunit of myosin phosphatase. Y27632 markedly prevented neointima formation at days 7 and 14. In controls, BrdU + proliferating and TUNEL + apoptotic SMCs were transiently and coincidentally increased in the neointima, with a peak at day 7. Y27632 significantly increased the neointimal TUNEL + SMCs at days 7 and 14, but not BrdU + SMCs. Y27642 significantly decreased the number of intimal SMCs at day 4, while not affecting the number of BrdU + or TUNEL + SMCs. Reendothelialization after balloon injury was not significantly affected by Y27632 at days 7 and 14. Conclusions —Y27632 inhibited neointima formation by enhancing SMC apoptosis and probably by suppressing early SMC migration. Therefore, a role of Rho-kinase is suggested in neointima formation after vascular injury.

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“…In a preclinical study, Ishizaka et al (2) evaluated the effect of locally administered cilostazol on neointimal formation in the balloon-injured rat carotid artery. The intimal area of the injured carotid was significantly smaller in the cilostazol-treated group than in the control group (0.06±0.01 mm 2 versus 0.15±0.02 mm 2 ; P<0.001).…”

Section: Antiproliferative Effectsmentioning

confidence: 99%

“…Cilostazol was shown to decrease the rate of restenosis in major subgroups, including patients with diabetes and small vessels. The mechanism by which cilostazol decreased restenosis is not clear, but may be related to decreased cellular proliferation (2)(3)(4).…”

Section: Inhibition Of Restenosis After Coronary Stent Implantationmentioning

confidence: 99%

The vascular effects of cilostazol

Weintraub

2006

Canadian Journal of Cardiology

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Effects of a single local administration of cilostazol on neointimal formation in balloon-injured rat carotid artery

Cited by 82 publications

References 22 publications

Inhibition of neointimal formation after balloon injury by cilostazol, accompanied by improvement of endothelial dysfunction and induction of hepatocyte growth factor in rat diabetes model

Inhibition of neointimal formation after balloon injury by cilostazol, accompanied by improvement of endothelial dysfunction and induction of hepatocyte growth factor in rat diabetes model

Role of Rho-Associated Kinase in Neointima Formation After Vascular Injury

The vascular effects of cilostazol

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