Circulating immunoreactive endothelin in patients undergoing percutaneous transluminal coronary angioplasty

Tahara, Akira; Kohno, Masakazu; Yanagi, Shiro; Itagane, Hiroshi; Toda, Iku; Akioka, Kaname; Teragaki, Masakazu; Yasuda, Mitsutaka; Takeuchi, Kazuhide; Takeda, Tadanao

doi:10.1016/0026-0495(91)90021-n

Cited by 71 publications

(16 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Endothelin-1 (ET1) is a contractile and growth-promoting vasoactive agonist that is released in response to endothelial injury and is thought to be important in the dysregulation of smooth muscle cell growth in disease states such as angioplasty-induced restenosis and pulmonary hypertension (Tahara et al, 1991;Giaid et al, 1993). ET1 stimulates SRF activity via the heterotrimeric G proteins G q/11 and G 12/13 , with subsequent downstream activation of the small GTPase RhoA, polymerization of monomeric G-actin to filamentous F actin, and subsequent transactivation of SRF (Gohla et al, 1999;Sotiropoulos et al, 1999).…”

mentioning

confidence: 99%

Regulation of Serum Response Factor-Dependent Gene Expression by Proteasome Inhibitors

Sandbo

Qin²,

Taurin³

et al. 2004

Mol Pharmacol

View full text Add to dashboard Cite

Serum response factor (SRF) is activated by contractile and hypertrophic agonists, such as endothelin-1 (ET1) to stimulate expression of cytoskeletal proteins in vascular smooth muscle cells (VSMCs). While studying the regulation of smooth muscle ␣-actin (SMA) expression at the level of protein stability, we discovered that inhibition of proteasome-dependent protein degradation by N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) or lactacystin (LC) did not enhance the levels of SMA, but, unexpectedly, attenuated SMA expression in response to ET1, without affecting the viability of VSMCs. Down-regulation of SMA protein by MG132 or LC occurred at the level of SMA transcription and via the inhibition of SRF activity. By contrast, MG132 and LC potentiated the activity of activator protein-1 transcription factor. Regulation of SRF by MG132 was not related to inhibition of nuclear factor-B, an established target of proteasome inhibitors, and was not mediated by protein kinase A, a powerful regulator of SRF activity. Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding. MG132 treatment did not result in ubiquitination or accumulation of SRF. By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity. Together, these data suggest that inhibition of proteasome results in down-regulation of SMA expression via up-regulation of c-Jun and repression of SRF activity at the level of DNA binding.

show abstract

mentioning

confidence: 99%

Regulation of Serum Response Factor-Dependent Gene Expression by Proteasome Inhibitors

Sandbo

Qin²,

Taurin³

et al. 2004

Mol Pharmacol

View full text Add to dashboard Cite

show abstract

“…3 Since levels of endothelin-1 are elevated in the human coronary sinus after PTCA, it has been suggested that endothelin-1 is involved in the pathogenesis of vascular restenosis. 4 In addition to its actions on vascular smooth muscle tonus, endothelin-1 is also a potent mitogen in several cultured cell lines of both cardiovascular and noncar-growth factors, the latter of which may be synergistic. [6][7][8][9][10] However, despite these in vitro observations, the in vivo role of endothelin-1 as a mitogen is unknown, since results from cell culture are often difficult to interpret (eg, because of the absence of blood-borne factors and interactions between different cell types) and may not translate into an in vivo situation.…”

mentioning

confidence: 99%

A role for endogenous endothelin-1 in neointimal formation after rat carotid artery balloon angioplasty. Protective effects of the novel nonpeptide endothelin receptor antagonist SB 209670.

Douglas

Louden

Vickery-Clark

et al. 1994

Circulation Research

172

View full text Add to dashboard Cite

The observation that levels of the mitogenic peptide endothelin-1 are elevated in the human coronary sinus after percutaneous transluminal coronary angioplasty (PTCA) has implicated endothelin-1 in the etiology of vascular restenosis. The present study examined this hypothesis in both an in vitro and an in vivo rat model of neointimal formation by using the novel nonpeptide endothelin receptor antagonist SB 209670. In vitro, endothelin-1 (1 nmol/L) induced a ninefold increase in rat aortic vascular smooth muscle [3Hlthymidine incorporation. This endothelin A receptor-mediated effect was completely inhibited by SB 209670 (IC50, 6.2±2.2 nmol/L). In vivo, acute intra-arterial administration of exogenous endothelin-1 (5 to 500 pmol/kg over a 30-minute period immediately after angioplasty) dose-dependently augmented the degree of neointimal formation (by up to 150% when assessed 14 days after surgery). This response was evident as early as 7 days after angioplasty. Hemodynamic studies indicated that this action was unrelated to a systemic pressor action of the peptide. Administration of SB 209670 (2.5 mg/kg IP, twice a day for 3 days before and for 2 weeks after surgery) reduced neointimal formation by '50% relative to control animals. Thus, the data indicate for the first time that (1) endothelin-1 promotes neointimal formation in vivo and (2) tensin II and norepinephrine, endothelin-1 is now recognized as playing an intrinsic role in the endogenous control of systemic hemodynamics.3 Since levels of endothelin-1 are elevated in the human coronary sinus after PTCA, it has been suggested that endothelin-1 is involved in the pathogenesis of vascular restenosis.4In addition to its actions on vascular smooth muscle tonus, endothelin-1 is also a potent mitogen in several cultured cell lines of both cardiovascular and noncarReceived February 1, 1994; accepted March 21, 1994.

show abstract

“…32 Human atherosclerotic plaque demonstrates a highly significant increase in both big ET and ET compared with histologically normal vessel, with dense binding of ET-1 observed in medial smooth muscle cells of normal and diseased aorta by autoradiography. 12 ET-1 immunoreactivity is increased after coronary angioplasty in patients, both in the coronary sinus 13 and in the distal segment of the injured artery. 14 The level of reactivity correlates with the degree of mechanical stress applied to the arterial lesion.…”

Section: Discussionmentioning

confidence: 96%

“…12 This evidence suggests that ET, via binding to ET A receptors, stimulates vascular smooth muscle cell proliferation and thus may be pivotally involved in the pathogenesis of atherosclerosis. ET-1 immunoreactivity is also increased in patients after coronary angioplasty, both in the coronary sinus 13 and in the distal segment of the injured artery. 14 The level of reactivity correlates with the degree of mechanical stress applied to the arterial lesion.…”

mentioning

confidence: 94%

Selective ETA Receptor Antagonism Reduces Neointimal Hyperplasia in a Porcine Coronary Stent Model

McKenna¹

1998

Journal of the American College of Cardiology

View full text Add to dashboard Cite

Background-As endothelin binds to ET A receptors, it stimulates vascular smooth muscle cell proliferation and may thus be pivotally involved in the pathogenesis of restenosis. This study assessed the ability of a potent and selective ET A antagonist to reduce neointimal hyperplasia in a porcine coronary artery stented injury model. Methods and Results-Fifty-five pigs were randomized to receive placebo or the oral ET A -selective antagonist ABT147627 twice daily for 28 days in one of three doses: 0.75 mg/kg (low), 3.75 mg/kg (mid), and 10.0 mg/kg (high). Each underwent oversized stent deployment in two randomly assigned major epicardial coronary arteries. Three animals (5.5%) died as a consequence of stent thrombosis within 24 hours of the procedure. The remaining 52 animals (13 pigs per group) survived without complication until predetermined euthanasia at 28 days. In the placebo group, mean injury score was 1.

show abstract

Circulating immunoreactive endothelin in patients undergoing percutaneous transluminal coronary angioplasty

Cited by 71 publications

References 6 publications

Regulation of Serum Response Factor-Dependent Gene Expression by Proteasome Inhibitors

Regulation of Serum Response Factor-Dependent Gene Expression by Proteasome Inhibitors

A role for endogenous endothelin-1 in neointimal formation after rat carotid artery balloon angioplasty. Protective effects of the novel nonpeptide endothelin receptor antagonist SB 209670.

Selective ETA Receptor Antagonism Reduces Neointimal Hyperplasia in a Porcine Coronary Stent Model

Contact Info

Product

Resources

About