Suppression of Cell Proliferation by Tissue Plasminogen Activator During the Early Phase After Balloon Injury Minimizes Intimal Hyperplasia in Hypercholesterolemic Rabbits

Kanamasa, Ken; Otani, Narutaka; Ishida, Norihiro; Inoue, Yoshikazu; Ikeda, Akiko; Morii, H.; Naito, Norikatsu; Hayashi, Tetsuo; Ishikawa, Kinji; Miyazawa, Masaaki

doi:10.1097/00005344-200102000-00003

Cited by 10 publications

(6 citation statements)

References 30 publications

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“…t-PA-mediated plasmin generation can also be regulated by thrombin [64]. In addition to its role in fibrinolysis, t-PA expression is down regulated by shear stress, which is consistent with the known tendency of low shear stress and/or disturbed flow areas within the vasculature resulting in thrombus formation and vascular cell proliferation [65,66]. Recently, t-PA signaling and subsequent downstream mitogenic events has been found to depend on the activation of the sphingosine-1-phosphate signaling pathway.…”

Section: T-pasupporting

confidence: 55%

“…Conversely, a lack of u-PA leads to a reduction in neointimal hyperplasia. Surprisingly, infusion of t-PA after arterial injury appears to decrease medial cell proliferation and suppress intimal hyperplasia in a rabbit model of hypercholesterolemia [66]. This may be associated with reduction in mural thrombus burden and earlier recovery of endothelial cell coverage.…”

Section: Restenosismentioning

confidence: 88%

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Plasminogen Activator System and Vascular Disease

Nicholl¹,

Roztocil²,

Davies³

2006

CVP

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Vascular diseases, such as atherosclerosis, thromboembolic disorders and stroke, in addition to surgical procedures such as restenosis, all share the plasminogen activator system as a central component in the pathogenesis of vascular injury. Since the development of plasminogen deficient mice our knowledge of the effects of this proteolytic system in cardiovascular disease has vastly increased. The plasminogen activator system plays a key role in vascular homeostasis and constitutes a critical response mechanism to cardiovascular injury. The central components of the PA system are the proteolytic activators, urokinase-plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA), plasminogen (plg) and its degradation product, plasmin, together with the major inhibitors of this system, plasminogen activator inhibitor-1 and -2 (PAI-1, PAI-2). An extensive network of additional proteases, inhibitors, receptors and modulators directly associate and are influenced by the PA system, the largest group being the Matrix Metalloproteinases (MMPs) and their respective inhibitors the Tissue inhibitors of MMPs (TIMPS).

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Section: T-pasupporting

confidence: 55%

Section: Restenosismentioning

confidence: 88%

Plasminogen Activator System and Vascular Disease

Nicholl¹,

Roztocil²,

Davies³

2006

CVP

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“…endothelial denudation by a Fogarty catheter) and subsequent feeding of a high-cholesterol diet. 88 Rabbit models serve as single-, double-or tripleinjury models, which can be induced as biochemical damage with hypercholesterolaemic diets, or as mechanical injury through either balloon catheter or air dessication bilaterally in the femoral artery. 87 The stenotic lesions induced by this technique predominantly consisted of lipid-laden foam cells, which are frequently found in human plaques.…”

Section: Rabbit Iliac Modelmentioning

confidence: 99%

Impact of metabolic syndrome on re-stenosis development: Role of drug-eluting stents

Goyal

Bharti

Krishnamurthy

et al. 2012

Diabetes and Vascular Disease Research

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Metabolic syndrome (MetS) is defined as a cluster of numerous cardiovascular risk factors, which encompasses obesity, dyslipidaemia, insulin resistance and hypertension. Patients with MetS are more prone to developing cardiovascular events than other patients. To date, several approaches such as physical exercise, dietary control and invasive and non-invasive therapeutic interventions for dyslipidaemia, hypertension and insulin resistance have been used to manage MetS. However, there is a progressive elevation in the incidence of fatal and non-fatal cardiovascular events due to the increased prevalence of obesity and diabetes. Percutaneous coronary intervention has emerged over the last few years as an effective revascularisation strategy for those with coronary artery disease, in parallel with the development of effective anti-platelet medications and newer drug-eluting stents. In recent years, considerable research efforts have been undertaken to elucidate the pathophysiology of re-stenosis and develop strategies to prevent re-stenosis following percutaneous transluminal coronary angioplasty and stent implantation. Although the rate of stent re-stenosis and target-lesion revascularisation has been reduced, there is little information in the literature on the outcome of MetS in the pathophysiology of re-stenosis. In this review article, we summarise the recent development and progress on re-stenosis and the role of drug-eluting stents, particularly in MetS.

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“…(30). Infusion of tPA after arterial injury appears to decrease medial cell proliferation and suppress intimal hyperplasia (31). This may be associated with reduction in mural thrombus burden and earlier recovery of endothelial cell coverage.…”

Section: Plasminogen Activationmentioning

confidence: 99%