Replication of smooth muscle cells in vascular disease.

Schwartz, Stephen M.; Campbell, Gordon; Campbell, Julie H.

doi:10.1161/01.res.58.4.427

Cited by 680 publications

(392 citation statements)

References 159 publications

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“…This is underscored by the observation that a microsatellite polymorphism in the promoter region of the HO-1 gene that is linked to decreased inducibility is associated with restenosis and increased vascular inflammation after percutaneous transluminal angioplasty, susceptibility to coronary artery disease in type 2 diabetic patients and in Japanese patients with coronary risk factors, and the development of abdominal aortic aneurysms (Exner et al, 2001;Chen et al, 2002;Kaneda et al, 2002;Schillinger et al, 2002a,b). Since excessive growth of vascular SMCs is an important contributing factor to a number of vascular disease states, including restenosis following angioplasty, atherosclerosis, and hypertension (Zierler et al, 1982;Ross, 1986;Schwartz et al, 1986), increasing HO-1 expression in blood vessels may offer a promising approach in treating vascular disorders. As shown in Figure 2, the expression of HO-1 in SMCs may block the growth of vascular SMCs via multiple mechanisms.…”

Section: Ho-1 As a Therapeutic Target In Vascular Diseasementioning

confidence: 99%

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

Durante

2003

Journal Cellular Physiology

143

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Heme oxygenase-1 (HO-1) catalyzes the degradation of heme to carbon monoxide (CO), iron, and biliverdin. Biliverdin is subsequently metabolized to bilirubin by the enzyme biliverdin reductase. Although interest in HO-1 originally centered on its heme-degrading function, recent findings indicate that HO-1 exerts other biologically important actions. Emerging evidence suggests that HO-1 plays a critical role in growth regulation. Deletion of the HO-1 gene or inhibition of HO-1 activity results in growth retardation and impaired fetal development, whereas HO-1 overexpression increases body size. Although the mechanisms responsible for the growth promoting properties of HO-1 are not well established, HO-1 can indirectly influence growth by regulating the synthesis of growth factors and by modulating the delivery of oxygen or nutrients to specific target tissues. In addition, HO-1 exerts important effects on critical determinants of tissue size, including cell proliferation, apoptosis, and hypertrophy. However, the actions of HO-1 are highly variable and may reflect a role for HO-1 in maintaining tissue homeostasis. Considerable evidence supports a crucial role for HO-1 in blocking the growth of vascular smooth muscle cells (SMCs). This antiproliferative effect of HO-1 is mediated primarily via the release of CO, which inhibits vascular SMC growth via multiple pathways. Pharmacologic or genetic approaches targeting HO-1 or CO to the blood vessel wall may represent a promising, novel therapeutic approach in treating vascular proliferative disorders.

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Section: Ho-1 As a Therapeutic Target In Vascular Diseasementioning

confidence: 99%

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

Durante

2003

Journal Cellular Physiology

143

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“…The proliferation of smooth muscle cells in vitro is stimulated by various mitogens such as PDGF, IGF-1, basic fibroblast growth factor, EGF, IL-1, and TGF-f3 (1)(2)(3). The binding of growth factors to specific receptors on smooth muscle cells initiates a complicated series of biochemical reactions which involve protein kinase C, receptor-linked tyrosine phosphorylation, and cAMP-dependent kinases (4).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, the growth response in a number of cell types, including smooth muscle cells, to serum mitogens in vitro is suppressed by antisense oligonucleotides directed against c-myc, c-myb, proliferating cell nuclear antigen (PCNA),' cyclins, and non- 1. Abbreviations used in this paper: PCNA, proliferating cell nuclear antigen; SV40LT-SMC, smooth muscle cell line immortalized with SV40 large T antigen.…”

Section: Introductionmentioning

confidence: 99%

Antisense proliferating cell nuclear antigen oligonucleotides inhibit intimal hyperplasia in a rat carotid artery injury model.

Simons

Edelman²,

Rosenberg³

1994

J. Clin. Invest.

111

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We have used antisense phosphorothioate oligonucleotides to define the role played by proliferating cell nuclear antigen (PCNA) in neointimal accumulation of smooth muscle cells in a rat carotid artery injury model. The short-term extraluminal delivery of 250 nmol of antisense oligonucleotides, but not control oligonucleotides, immediately after arterial injury produces a 77% suppression of PCNA mRNA after 24 h and a 52% decrease in the frequency of medial smooth muscle cells expressing PCNA after 72 h. This reduction in PCNA expression is accompanied by a 59% decrease in the frequency of proliferating medial smooth muscle cells at 3 d as measured by BudR staining and an 80% decrease in neointimal accumulation assessed morphometrically at 2 wk. Thus, the expression of PCNA is required for medial smooth muscle cell growth in vivo and for neointimal formation after arterial injury. (J. Clin. Invest. 1994Invest. . 93:2351Invest. -2356

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“…Dedifferentiation of vascular smooth muscle cells (VSMCs), followed by their migration from media to intima and proliferation in intima, contribute to the pathophysiology of renarrowing of the artery after angioplasty (15,16). Previously, we have shown that NFATs play a role in the regulation of VSMC growth and migration (17,18).…”

mentioning

confidence: 99%

Cyclin D1 Is a Bona Fide Target Gene of NFATc1 and Is Sufficient in the Mediation of Injury-induced Vascular Wall Remodeling

Karpurapu

Wang

Quyền

et al. 2010

Journal of Biological Chemistry

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Platelet-derived growth factor BB induced cyclin D1 expression in a time-and nuclear factor of activated T cells (NFAT)-dependent manner in human aortic smooth muscle cells (HASMCs), and blockade of NFATs prevented HASMC DNA synthesis and their cell cycle progression from G 1 to S phase. Selective inhibition of NFATc1 by its small interfering RNA also blocked HASMC proliferation and migration. Characterization of the cyclin D1 promoter revealed the presence of several NFAT binding sites, and the site at nucleotide ؊1333 was found to be sufficient in mediating platelet-derived growth factor BBinduced cyclin D1 promoter-luciferase reporter gene activity. In addition to its role in cell cycle progression, cyclin D1 mediated HASMC migration in an NFATc1-dependent manner. Balloon injury-induced cyclin D1-CDK4 activity requires NFAT activation, and adenovirus-mediated transduction of cyclin D1 was found to be sufficient to overcome the blockade effect of NFATs by VIVIT on balloon injury-induced vascular wall remodeling events, including smooth muscle cell migration from the medial to luminal region, their proliferation in the intimal region, and neointima formation. Together, these results provide more mechanistic evidence for the role of NFATs, particularly NFATc1, in the regulation of HASMC proliferation and migration as well as vascular wall remodeling. NFATc1 could be a potential therapeutic target against the renarrowing of artery after angioplasty.

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Replication of smooth muscle cells in vascular disease.

Cited by 680 publications

References 159 publications

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

Heme oxygenase‐1 in growth control and its clinical application to vascular disease

Antisense proliferating cell nuclear antigen oligonucleotides inhibit intimal hyperplasia in a rat carotid artery injury model.

Cyclin D1 Is a Bona Fide Target Gene of NFATc1 and Is Sufficient in the Mediation of Injury-induced Vascular Wall Remodeling

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