Migration of smooth muscle and endothelial cells. Critical events in restenosis.

Casscells, Ward

doi:10.1161/01.cir.86.3.723

Cited by 341 publications

(176 citation statements)

References 68 publications

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“…tion process. Another population of medial SMCs just migrates without DNA synthesis (21,22). Therefore, the results of the present study suggest that SMCs have functional μ-opioid receptors whose signal transduction pathway interferes with both proliferation and migration.…”

Section: Discussionmentioning

confidence: 60%

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

et al. 2008

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Section: Discussionmentioning

confidence: 60%

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

et al. 2008

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“…E xcessive vascular smooth muscle cell (SMC) proliferation is a feature of restenosis after percutaneous coronary interventions and is present in spontaneous atherosclerotic lesions (Casscells, 1992;Foegh and Virmani, 1993;Ross, 1999). Control of cell proliferation by targeting cell-cycle regulation has been proposed as a therapeutic strategy to prevent development of intimal hyperplasia (Braun-Dullaeus et al, 1998;Chang et al, 1995;Chen et al, 1997;Li and Brooks, 1999;MacLellan and Majesky, 1997;Mann et al, 1999;Morishita et al, 1994.…”

Section: Discussionmentioning

confidence: 99%

Effect of p27 Deficiency and Rapamycin on Intimal Hyperplasia: In Vivo and In Vitro Studies Using a p27 Knockout Mouse Model

Roqué

Reis

Cordon‐Cardo

et al. 2001

Laboratory Investigation

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SUMMARY:Rapamycin, an immunosuppressant and antiproliferative agent, reduces intimal hyperplasia after arterial injury in animal models and in a preliminary study in humans. Rapamycin treatment reportedly increases expression of p27, a cyclin-dependent kinase inhibitor. This mechanism was tested using a p27-deficient (p27 Ϫ/Ϫ) murine model. Aortic smooth muscle cells from wild-type (WT) and p27 Ϫ/Ϫ mice were isolated and cultured. Cell proliferation, assessed by cell count and 3 H-thymidine incorporation, was inhibited significantly by rapamycin in WT and p27 Ϫ/Ϫ cells at concentrations of 1 ng/ml, 10 ng/ml, and 100 ng/ml (p Ͻ 0.05, versus control). The in vivo effect on intimal hyperplasia was studied in p27 Ϫ/Ϫ and WT mice after femoral artery transluminal injury. Rapamycin treatment was started 2 days before injury and maintained for 2 weeks (1 mg/kg per 48 hours, ip). No significant differences in intima-to-media ratio were found between WT (1.1 Ϯ 0.1) and p27 Ϫ/Ϫ mice (1.0 Ϯ 0.1) 4 weeks after injury. Rapamycin significantly (p Ͻ 0.05) reduced intima-to-media ratios in both WT (0.7 Ϯ 0.1) and p27 Ϫ/Ϫ mice (0.5 Ϯ 0.1), compared with untreated mice. p27 deficiency did not alter the arterial wall proliferative response to injury. The inhibitory effect of rapamycin on intimal hyperplasia occurred via a p27-independent mechanism. The in vitro data showed that this effect was mediated through decreased proliferation and enhanced apoptosis. (Lab Invest 2001, 81:895-903).E xcessive vascular smooth muscle cell (SMC) proliferation is a feature of restenosis after percutaneous coronary interventions and is present in spontaneous atherosclerotic lesions (Casscells, 1992;Foegh and Virmani, 1993;Ross, 1999). Control of cell proliferation by targeting cell-cycle regulation has been proposed as a therapeutic strategy to prevent development of intimal hyperplasia (Braun-Dullaeus et al, 1998;Chang et al, 1995;Chen et al, 1997;Li and Brooks, 1999;MacLellan and Majesky, 1997;Mann et al, 1999;Morishita et al, 1994.Cyclin-dependent kinase inhibitors (CDKIs) are critical regulators of cell-cycle progression. These proteins bind to complexes formed by cyclins and cyclindependent kinases (CDKs), inhibiting their enzymatic activity and thereby inducing cell-cycle arrest (Sherr and Roberts, 1995). p27 kip1 is an ubiquitous CDKI with a predominant role in regulating G1/S phase transition, determining cell entry into S phase or withdrawal from the cycle (Koff et al, 1993;Polyak et al, 1994).Mitogenic stimuli, such as platelet-derived growth factor (PDGF) and interleukin-2, down-regulate p27 (Nourse et al, 1994). Low intracellular levels of free p27 enable retinoblastoma protein (pRB) hyperphosphorylation by cyclin-CDK complexes, subsequent release of E2F transcription factor, and cell replication .Rapamycin is a potent growth inhibitor that impairs progression through G1/S transition (Marx et al, 1995). Proposed mechanisms of action include inhibition of p70S6 kinase, impairment of pRB hyperphosphorylation, and prevention of p27 down-r...

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“…The pathogenesis of restenosis is multifactorial, involving such events as endothelial injury, inflammation, platelet activation, and hyperplasia of the intima, primarily due to vascular smooth muscle cell replication (vSMC). 3 The incidence of intimal hyperplasia varies in different risk populations, e.g., diabetic patients, up to 35% of whom require bare metal stent implantation; clinical evidence has shown that this value is reduced but continues to cause problems after the implantation of drug-eluting stents (DES) 4 .…”

Section: Introductionmentioning

confidence: 99%

A successful experimental model for intimal hyperplasia prevention using a resveratrol-delivering balloon

Tolva

Mazzola

Zerbi

et al. 2016

Journal of Vascular Surgery

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Migration of smooth muscle and endothelial cells. Critical events in restenosis.

Cited by 341 publications

References 68 publications

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

Effect of p27 Deficiency and Rapamycin on Intimal Hyperplasia: In Vivo and In Vitro Studies Using a p27 Knockout Mouse Model

A successful experimental model for intimal hyperplasia prevention using a resveratrol-delivering balloon

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