Randomized double-blind Scandinavian trial of angiopeptin versus placebo for the prevention of clinical events and restenosis after coronary balloon angioplasty

Eriksen, Ulrik; Amtorp, Ole; Bagger, Jens Peder; Emanuelsson, H; Foegh, Marie L.; Henningsen, P; Saunamäki, Kari; M, Schaeffer; Thayssen, Per; Ørskov, Hans; Kuntz, Richard E.; Popma, Jeffrey J.

doi:10.1016/0002-8703(95)90227-9

Cited by 78 publications

(35 citation statements)

References 21 publications

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“…Two smaller studies of 80 and 455 patients 13,14 have been inconclusive, whereas a larger study of 1246 patients 15 showed no significant effect on clinical events and restenosis rates. Where somatostatin analogues exhibit real benefit is in the setting of heart transplant vasculopathy 16,17 ; here, however, the drug's efficacy may rely on the distinct, largely immunomediated, pathogenesis of graft versus host arterial disease, 18 involving a reduction of the immunoenhancing actions of IGF-1-and VEGF.…”

Section: Igf-1: Vascular Detrimental Factor?mentioning

confidence: 95%

Insulin-Like Growth Factor-1 as a Vascular Protective Factor

Conti¹,

Carrozza²,

Capoluongo³

et al. 2004

Circulation

229

162

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Section: Igf-1: Vascular Detrimental Factor?mentioning

confidence: 95%

Insulin-Like Growth Factor-1 as a Vascular Protective Factor

Conti¹,

Carrozza²,

Capoluongo³

et al. 2004

Circulation

229

162

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“…100 However, clinical trials show that octreotide has no benefit, 101 and the effects of angiopeptin on restenosis are equivocal. [102][103][104] This discrepancy could be due to different doses and treatment regimes. It is important to note that an inhibitory stable D-peptide analogue of IGF-1 inhibits VSMC proliferation after rat carotid artery balloon injury, consistent with a role for IGF-1 in the restenotic process.…”

Section: Restenosismentioning

confidence: 99%

Expression, Regulation, and Function of IGF-1, IGF-1R, and IGF-1 Binding Proteins in Blood Vessels

Delafontaine

Song

2004

ATVB

487

374

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Abstract-The vascular insulin-like growth factor (IGF)-1 system includes the IGFs, the IGF-1 receptor (IGF-1R), and multiple binding proteins. This growth factor system exerts multiple physiologic effects on the vasculature through both endocrine and autocrine/paracrine mechanisms. The effects of IGF-1 are mediated principally through the IGF-1R but are modulated by complex interactions with multiple IGF binding proteins that themselves are regulated by phosphorylation, proteolysis, polymerization, and cell or matrix association. During the last decade, a significant body of evidence has accumulated, indicating that expression of the components of the IGF system are regulated by multiple factors, including growth factors, cytokines, lipoproteins, reactive oxygen species, and hemodynamic forces. In addition, cross-talk between the IGF system and other growth factors and integrin receptors has been demonstrated. There is accumulating evidence of a role for IGF-1 in multiple vascular pathologies, including atherosclerosis, hypertension, restenosis, angiogenesis, and diabetic vascular disease. This review will discuss the regulation of expression of IGF-1, IGF-1R, and IGF binding proteins in the vasculature and summarize evidence implicating involvement of this system in vascular diseases.

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“…The peptide hormone somatostatin induces numerous biological actions, most of which are inhibitory, by interacting with cell membrane receptors of which five types, named sst [1][2][3][4][5] , have been heterologously expressed in different cells within the last few years (1). The growth inhibitory effects of somatostatin are well documented as it is considered to be the physiological regulator of growth hormone release (2).…”

mentioning

confidence: 99%

Prolonged Activation of Extracellular Signal-regulated Kinase by a Protein Kinase C-dependent and N17Ras-insensitive Mechanism Mediates the Proliferative Response of Gi/o-coupled Somatostatin sst4 Receptors

Sellers

1999

Journal of Biological Chemistry

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The human sst 4 receptor, recombinantly expressed in Chinese hamster ovary cells, mediates proliferative activity of the peptide hormone somatostatin. This effect was shown to involve activation of pertussis toxin-sensitive G proteins and was inhibited by overexpression of the ␤␥-sequestrant, transducin. Somatostatin-induced proliferation was abolished by the MEK1 inhibitor, PD 98059, whereas the Src inhibitor, PP1, had no effect. A marked increase was observed in the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1 and ERK2) 10 min after sst 4 receptor activation, which was blocked by pertussis toxin, decreased by PP1 and the ␤␥-sequestrant, but unaffected by PD 98059. In contrast, the somatostatin-induced phosphorylation of ERK obtained at 4 h, although sensitive to both pertussis toxin and transducin, was unaffected by PP1 but ablated by PD 98059. Protein kinase C inhibition also abolished this somatostatin-induced sustained phosphorylation of ERK, together with the associated increase in cell proliferation. Expression of dominant negative Ras (N17) failed to significantly reduce the proliferative effect mediated by the sst 4 receptor but markedly attenuated the acute phase of the somatostatin-induced phosphorylation of ERK obtained at 10 min. In contrast, the phosphorylation induced at 4 h was unaffected. We conclude that ERK activation by G i/o -coupled sst 4 receptors involves a Src and Ras-dependent acute phase, but the proliferative response is dependent upon the prolonged ERK-induced activity, mediated by protein kinase C.

show abstract

Randomized double-blind Scandinavian trial of angiopeptin versus placebo for the prevention of clinical events and restenosis after coronary balloon angioplasty

Cited by 78 publications

References 21 publications

Insulin-Like Growth Factor-1 as a Vascular Protective Factor

Insulin-Like Growth Factor-1 as a Vascular Protective Factor

Expression, Regulation, and Function of IGF-1, IGF-1R, and IGF-1 Binding Proteins in Blood Vessels

Prolonged Activation of Extracellular Signal-regulated Kinase by a Protein Kinase C-dependent and N17Ras-insensitive Mechanism Mediates the Proliferative Response of Gi/o-coupled Somatostatin sst4 Receptors

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