IGF-1 expression in infarcted myocardium and MGF E peptide actions in rat cardiomyocytes in vitro (original) (raw)
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Vascular cell, 2011
Coronary artery disease is a global health concern in the present day with limited therapies. Extensive efforts have been devoted to find molecular therapies to enhance perfusion and function of the ischemic myocardium. Aim of the present study was to look into the effects of insulin like growth factor -1 (IGF-1) on circulating angiogenic factors after myocardial ischemia in rats. Adult male Sprague-Dawley rats were randomly divided into 10-days control, myocardial infarction, IGF-1 alone (2 μg/rat/day) and ISO+IGF-1 groups. Isoproterenol (ISO), a synthetic catecholamine was used to induce myocardial infarction. Serum transforming growth factor-β (TGF-β) and vascular endothelial growth factor (VEGF) levels were checked after 10-days of IGF-1 administration. There was a significant increase in heart weight after IGF-1 treatment. A significant increase in cardiac enzyme level (CK-MB and LDH) was seen in isoproterenol treated rats when compared to control group. IGF-1treatment induced ...
Journal of Histochemistry & Cytochemistry, 2003
This study evaluated the effects of angiotensin-converting enzyme (ACE) inhibition after myocardial infarction (MI) on cardiac remodeling and gene expression and localization of components (ligands, receptors, and binding proteins) of the cardiac insulinlike growth factor (IGF) system. After ligation of the coronary artery, rats were randomized to vehicle or ACE inhibitor (Captopril, 50 mg/kg/day) for 4 weeks. Blood pressure, cardiac remodeling, and components of the IGF system were localized in the heart using in situ hybridization (ISH) and immunohistochemistry (IHC). The average infarct size was 42%. There were regional differences in the expression of the IGF system after MI, with increased IGF-I mRNA abundance in the border (24-fold) and infarct (12-fold) and increased IGF-binding protein (IGFBP)-3 mRNA in all areas of the failing left ventricle (threefold). Captopril reduced blood pressure, attenuated cardiac remodeling, and caused a threefold increase in IGF-I receptor mRNA a...
Markedly reduced insulin-like growth factor-1 in the acute phase of myocardial infarction
Journal of the American College of Cardiology, 2001
We investigated whether insulin-like growth factor-1 (IGF-1) is reduced in the early phase of acute myocardial infarction (AMI) and whether such a decrease might influence prognosis. BACKGROUND Insulin-like growth factor-1 protects against insulin resistance and apoptosis. Although insulin resistance has been reported in AMI, IGF-1 levels have not been investigated.
Circulation. Cardiovascular interventions, 2011
Insulin-like growth factor-1 (IGF-1) is recognized as an important regulator of cardiac structure and cardiomyocyte homeostasis. The prosurvival and antiapoptotic effects of IGF-1 have been investigated in vitro and in rodent models of myocardial infarction (MI). However, the clinical application of IGF-1 has been hampered by dose-dependent side effects both acutely and during chronic administration. We hypothesized that single, low-dose IGF-1 (LD-IGF-1) administered locally and early in the reperfusion phase after acute MI in a large animal model would avoid significant side effects but would have prosurvival effects that would manifest in long-term structural and functional improvement after MI treatment. Forty-four female Landrace pigs underwent intracoronary administration of LD-IGF-1 or saline 2 hours into the reperfusion phase of acute left anterior descending artery occlusion MI. In the area of infarction, IGF-1 receptor and signaling responses were activated at 30 minutes an...
Journal of Clinical Investigation, 1997
Transgenic mice were generated in which the cDNA for the human insulin-like growth factor 1B (IGF-1B) was placed under the control of a rat a-myosin heavy chain promoter. In mice heterozygous for the transgene, IGF-1B mRNA was not detectable in the fetal heart at the end of gestation, was present in modest levels at 1 day after birth, and increased progressively with postnatal maturation, reaching a peak at 75 days. Myocytes isolated from transgenic mice secreted 1.15 + 0.25 ng of IGF-1 per 106 cells per 24 hr versus 0.27 ± 0.10 ng in myocytes from homozygous wild-type littermates. The plasma level of IGF-1 increased 84% in transgenic mice. Heart weight was comparable in wild-type littermates and transgenic mice up to 45 days of age, but a 42%, 45%, 62%, and 51% increase was found at 75, 135, 210, and 300 days, respectively, after birth. At 45, 75, and 210 days, the number of myocytes in the heart was 21%, 31%, and 55% higher, respectively, in transgenic animals. In contrast, myocyte cell volume was comparable in transgenic and control mice at all ages. In conclusion, overexpression of IGF-1 in myocytes leads to cardiomegaly mediated by an increased number of cells in the heart.
Insulin-like growth factor-1 in myocardial tissue: interaction with tumor necrosis factor
Critical care (London, England), 2003
Insulin-like growth factor (IGF)-1 is a well characterized growth factor that plays a role in the regulation of myocardial structure and function. Using an ex vivo murine model, Davani and coworkers, in this issue of Critical Care, demonstrate that IGF-1 confers cardiac protection against ischemia via mitochondria-dependent mechanisms. Those investigators used the ratio of mitochondrial to nuclear DNA to demonstrate that IGF-1, which prevents reduction in this ratio during reperfusion, provides cytoprotection. This commentary also reviews mechanisms of IGF-1 function and provides a graphic representation of IGF-1 signaling mechanisms in potential crosstalk relations with mediators of inflammation in the heart (specifically tumor necrosis factor-alpha).
Critical care (London, England), 2003
Ischemia/reperfusion occurs in myocardial infarction, cardiac dysfunction during sepsis, cardiac transplantation and coronary artery bypass grafting, and results in injury to the myocardium. Although reperfusion injury is related to the nature and duration of ischemia, it is also a separate entity that may jeopardize viable cells and ultimately may impair cardiac performance once ischemia is resolved and the organ heals. The present study was conducted in an ex vivo murine model of myocardial ischemia/reperfusion injury. After 20 min of ischemia, isolated hearts were perfused for up to 2 hours with solution (modified Kreb's) only, solution plus insulin-like growth factor (IGF)-1, or solution plus tumor necrosis factor (TNF)-alpha. Cardiac contractility was monitored continuously during this period of reperfusion. On the basis of histologic evidence, IGF-1 prevented reperfusion injury as compared with TNF-alpha; TNF-alpha increased perivascular interstitial edema and disrupted ti...
International journal of cardiovascular research, 2014
Insulin like growth factor-I (IGF-1) isoforms differ structurally in their E-domain regions and their temporal expression profile in response to injury. We and others have reported that Mechano-growth factor (MGF), which is equivalent to human IGF-1c and rodent IGF-1Eb isoforms, is expressed acutely following myocardial infarction (MI) in the mouse heart. To examine the function of the E-domain region, we have used a stabilized synthetic peptide analog corresponding to the unique 24 amino acid region E-domain of MGF. Here we deliver the human MGF E-domain peptide to mice during the acute phase (within 12 hours) and the chronic phase (8 weeks) post-MI. We assessed the impact of peptide delivery on cardiac function and cardiovascular hemodynamics by pressure-volume (P-V) loop analysis and gene expression by quantitative RT-PCR. A significant decline in both systolic and diastolic hemodynamics accompanied by pathologic hypertrophy occurred by 10 weeks post-MI in the untreated group. De...