Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells: A potential treatment for restenosis?

M. B. Grant, T. J. Wargovich, E. A. Ellis, S. Caballero, M. Mansour, C. J. Pepine

Research output: Contribution to journalArticle

163 Citations (Scopus)

Abstract

In this study, we demonstrate, for the first time, the localization of insulin-like growth factor I (IGF-I) in de novo and restenotic human coronary atherectomy plaques by using immunocytochemical techniques. Smooth muscle cells (SMCs) exhibiting the synthetic phenotype contained a statistically significant higher concentration of IGF-I than SMCs of the contractile phenotype or SMCs from normal coronary arteries. In addition, we provide data to suggest that the long-acting somatostatin analogues octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth factor (b-FGF)- induced human coronary artery SMC proliferation. Platelet-derived growth factor (PDGF)-stimulated cultures were minimally affected by the addition of octreotide but were significantly inhibited by angiopeptin. All three growth factors stimulated SMC migration in a dose-dependent manner. The somatostatin analogues tested had no effect on growth factor-stimulated SMC migration. Our data suggest that by reducing SMC proliferation, somatostatin analogues may have clinical usefulness in reducing the high incidence of restenosis observed after percutaneous transluminal coronary artery interventions.

Original languageEnglish (US)
Pages (from-to)1511-1517
Number of pages7
JournalCirculation
Volume89
Issue number4
StatePublished - Apr 1994
Externally publishedYes

Fingerprint

Somatostatin
Insulin-Like Growth Factor I
Smooth Muscle Myocytes
Growth
Coronary Vessels
Octreotide
Therapeutics
Cell Movement
Intercellular Signaling Peptides and Proteins
Cell Proliferation
Coronary Atherectomy
Phenotype
Platelet-Derived Growth Factor
Fibroblast Growth Factor 2
Incidence

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells : A potential treatment for restenosis? / Grant, M. B.; Wargovich, T. J.; Ellis, E. A.; Caballero, S.; Mansour, M.; Pepine, C. J.

In: Circulation, Vol. 89, No. 4, 04.1994, p. 1511-1517.

Research output: Contribution to journalArticle

@article{51882a9e605a40c4bda836d8090978af,
title = "Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells: A potential treatment for restenosis?",
abstract = "In this study, we demonstrate, for the first time, the localization of insulin-like growth factor I (IGF-I) in de novo and restenotic human coronary atherectomy plaques by using immunocytochemical techniques. Smooth muscle cells (SMCs) exhibiting the synthetic phenotype contained a statistically significant higher concentration of IGF-I than SMCs of the contractile phenotype or SMCs from normal coronary arteries. In addition, we provide data to suggest that the long-acting somatostatin analogues octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth factor (b-FGF)- induced human coronary artery SMC proliferation. Platelet-derived growth factor (PDGF)-stimulated cultures were minimally affected by the addition of octreotide but were significantly inhibited by angiopeptin. All three growth factors stimulated SMC migration in a dose-dependent manner. The somatostatin analogues tested had no effect on growth factor-stimulated SMC migration. Our data suggest that by reducing SMC proliferation, somatostatin analogues may have clinical usefulness in reducing the high incidence of restenosis observed after percutaneous transluminal coronary artery interventions.",
author = "Grant, {M. B.} and Wargovich, {T. J.} and Ellis, {E. A.} and S. Caballero and M. Mansour and Pepine, {C. J.}",
year = "1994",
month = "4",
language = "English (US)",
volume = "89",
pages = "1511--1517",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells

T2 - A potential treatment for restenosis?

AU - Grant, M. B.

AU - Wargovich, T. J.

AU - Ellis, E. A.

AU - Caballero, S.

AU - Mansour, M.

AU - Pepine, C. J.

PY - 1994/4

Y1 - 1994/4

N2 - In this study, we demonstrate, for the first time, the localization of insulin-like growth factor I (IGF-I) in de novo and restenotic human coronary atherectomy plaques by using immunocytochemical techniques. Smooth muscle cells (SMCs) exhibiting the synthetic phenotype contained a statistically significant higher concentration of IGF-I than SMCs of the contractile phenotype or SMCs from normal coronary arteries. In addition, we provide data to suggest that the long-acting somatostatin analogues octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth factor (b-FGF)- induced human coronary artery SMC proliferation. Platelet-derived growth factor (PDGF)-stimulated cultures were minimally affected by the addition of octreotide but were significantly inhibited by angiopeptin. All three growth factors stimulated SMC migration in a dose-dependent manner. The somatostatin analogues tested had no effect on growth factor-stimulated SMC migration. Our data suggest that by reducing SMC proliferation, somatostatin analogues may have clinical usefulness in reducing the high incidence of restenosis observed after percutaneous transluminal coronary artery interventions.

AB - In this study, we demonstrate, for the first time, the localization of insulin-like growth factor I (IGF-I) in de novo and restenotic human coronary atherectomy plaques by using immunocytochemical techniques. Smooth muscle cells (SMCs) exhibiting the synthetic phenotype contained a statistically significant higher concentration of IGF-I than SMCs of the contractile phenotype or SMCs from normal coronary arteries. In addition, we provide data to suggest that the long-acting somatostatin analogues octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth factor (b-FGF)- induced human coronary artery SMC proliferation. Platelet-derived growth factor (PDGF)-stimulated cultures were minimally affected by the addition of octreotide but were significantly inhibited by angiopeptin. All three growth factors stimulated SMC migration in a dose-dependent manner. The somatostatin analogues tested had no effect on growth factor-stimulated SMC migration. Our data suggest that by reducing SMC proliferation, somatostatin analogues may have clinical usefulness in reducing the high incidence of restenosis observed after percutaneous transluminal coronary artery interventions.

UR - http://www.scopus.com/inward/record.url?scp=0028314847&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028314847&partnerID=8YFLogxK

M3 - Article

C2 - 7908609

AN - SCOPUS:0028314847

VL - 89

SP - 1511

EP - 1517

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 4

ER -