Cardiac IGF-I manipulation by growth hormone following myocardial infarction

Matthews, Ken; Devlin, G.; Stuart, Selwyn; Conaglen, John V.; Bass, J. J.

doi:10.1016/j.ghir.2004.01.006

Cited by 13 publications

(11 citation statements)

References 50 publications

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“…The IGFs, namely IGF-1 and IGF-2, possess key roles in the regulation of fetal development throughout gestation by exerting metabolic, mitogenic and differentiative actions in a wide range of fetal tissues including the heart [15,16,18,19]. It has been suggested that both IGFs may act as progression mediators in cell cycle, DNA synthesis and cell differentiation in embryos and fetal cell lines [31,32].…”

Section: Discussionmentioning

confidence: 99%

“…Both IGF-1 and IGF-2 genes (Igf-1 and Igf-2) are expressed in fetal tissues from the earliest stage of pre-implantation development to the final phase of tissue maturation just prior to birth, with Igf-2 gene expression being more abundant than expression of the Igf-1 gene [14]. IGF-1 and IGF-2 have been shown to determine both normal and abnormal growth and development of many organ systems including heart and vasculature [15][16][17][18][19]. Mutation of the IGF-1 receptor or deletion of the Igf-1 gene retards intrauterine and postnatal growth while overexpression of the Igf-2 gene stimulates fetal overgrowth [20].…”

Section: Introductionmentioning

confidence: 99%

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Maternal nutrient restriction during early to mid gestation up-regulates cardiac insulin-like growth factor (IGF) receptors associated with enlarged ventricular size in fetal sheep

Dong

Ford

Fang

et al. 2005

Growth Hormone & IGF Research

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Maternal nutrient restriction during early to mid gestation up-regulates cardiac insulin-like growth factor (IGF) receptors associated with enlarged ventricular size in fetal sheep

Dong

Ford

Fang

et al. 2005

Growth Hormone & IGF Research

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“…A 4-week treatment with rhGH (0.67 mg/ kg), initiated immediately following LCAL, improved considerably cardiac function, in association with reduced pathological remodelling [24]. In a larger animal model, recombinant bovine GH (rbGH) elicited a dose-dependent cardiac hypertrophy following infarction, associated with an increased cardiac level of IGF-1 [25]. In contrast, an early treatment with rhGH (3 mg/kg per day for 3 weeks), starting 3 days post-surgery, attenuated LV remodelling without induction of LV hypertrophy in rats with large MI, an effect associated with an improved myocardial energy status, a decreased myocardial and plasma catecholamines and brain natriuretic peptide levels [26].…”

Section: Gh and Ghs In Experimental Heart Failurementioning

confidence: 99%

Cardiac and peripheral actions of growth hormone and its releasing peptides: Relevance for the treatment of cardiomyopathies

Marleau

Mulumba

Lamontagne

et al. 2006

Cardiovascular Research

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Ischemic and nonischemic cardiomyopathies are associated with significant morbidity and mortality in industrialized countries. Cardiomyopathies of primary origin, and more specifically the dilated form of the disease, have been associated with a number of gene defects in cytoskeletal, membrane, and sarcomeric proteins. Cardiomyopathies of secondary origin such as ischemic cardiomyopathy remain the leading cause of left ventricular systolic dysfunction and heart failure. Among novel strategies to improve cardiac function in heart failure, treatment with growth hormone, insulin growth factor-1 (IGF-1), and natural and synthetic growth hormone-releasing peptides such as ghrelin and hexarelin have been explored. The present review focuses on the issues involved in the use of exogenous growth hormone and its releasing peptides in experimental animal models of chronic heart failure and in clinical studies on cardiomyopathic patients as potential releasing peptides for the treatment of chronic heart failure developing as a consequence of cardiomyopathy.

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“…This locally produced IGF-I is now recognized as an important source for autocrine/paracrine signaling pathways that can regulate growth, proliferation, and survival. A recent study demonstrated that locally expressed cardiac IGF-I mRNA and protein can lead to physiological cardiomyocyte hypertrophy (30). It has also been reported that IGF-I produced by CFb can act as a local stimulant for cardiac hypertrophy and remodeling (15).…”

mentioning

confidence: 99%

An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts

Landeen²,

Aroonsakool³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Mechanical force can induce a number of fundamental short- and long-term responses in myocardium. These include alterations in ECM, activation of cell-signaling pathways, altered gene regulation, changes in cell proliferation and growth, and secretion of a number of peptides and growth factors. It is now known that a number of these autocrine/paracrine factors are secreted from both cardiomyocytes and ventricular cardiac fibroblasts (CFb) in response to stretch. One such substance is IGF-I. IGF-I is an important autocrine/paracrine factor that can regulate physiological or pathophysiological responses, such as hypertrophy. In this study, we addressed the possible effects of mechanical perturbation, biaxial strain, on IGF-I secretion from adult rat CFb. CFb were subjected to either static stretch (3–10%) or cyclic stretch (10%; 0.1–1 Hz) over a 24-h period. IGF-1 secretion from CFb in response to selected stretch paradigms was examined using ELISA to measure IGF-I concentrations in conditioned media. Static stretch did not result in any measurable modulation of IGF-I secretion from CFb. However, cyclic stretch significantly increased IGF-I secretion from CFb in a frequency- and time-dependent manner compared with nonstretched controls. This stretch-induced increase in secretion was relatively insensitive to changes in extracellular [Ca2+] or to block of L-type Ca2+ channels. In contrast, thapsigargin, an inhibitor of sarco(endo)plasmic reticulum Ca2+ ATPase, remarkably decreased stretch-induced IGF-I secretion from CFb. We further show that IGF-I can upregulate mRNA expression of atrial natriuretic peptide in myocytes. In summary, cyclic stretch can significantly increase IGF-I secretion from CFb, and this effect is dependent on a thapsigargin-sensitive pool of intracellular [Ca2+].

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Cardiac IGF-I manipulation by growth hormone following myocardial infarction

Cited by 13 publications

References 50 publications

Maternal nutrient restriction during early to mid gestation up-regulates cardiac insulin-like growth factor (IGF) receptors associated with enlarged ventricular size in fetal sheep

Maternal nutrient restriction during early to mid gestation up-regulates cardiac insulin-like growth factor (IGF) receptors associated with enlarged ventricular size in fetal sheep

Cardiac and peripheral actions of growth hormone and its releasing peptides: Relevance for the treatment of cardiomyopathies

An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts

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