IGF-1 expression in infarcted myocardium and MGF E peptide actions in rat cardiomyocytes in vitro

72Citations
Citations of this article
40Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Insulinlike growth factor-1 (IGF-1) expression is implicated in myocardial pathophysiology, and two IGF-1 mRNA splice variants have been detected in rodents, IGF-1Ea and mechano-growth factor (MGF). We investigated the expression pattern of IGF-1 gene transcripts in rat myocardium from 1 h up to 8 wks after myocardial infarction induced by left anterior descending coronary artery ligation. In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial- like cells in vitro. IGF-1Ea and MGF expression were significantly increased, both at transcriptional and translational levels, during the late postinfarction period (4 and 8 wks) in infarcted rat myocardium. Measurements of serum IGF-1 levels in infarcted rats were initially decreased (24 h up to 1 wk) but remained unaltered throughout the late experimental phase (4 to 8 wks) compared with sham-operated rats. Furthermore, specific anti-IGF-1R neutralizing antibody failed to block the synthetic MGF E peptide action, whereas it completely blocked IGF-1 action on the proliferation of H9C2 cells. Moreover, this synthetic MGF E peptide did not activate Akt phosphorylation, whereas it activated ERK1/2 in H9C2 rat myocardial cells. These data support the role of IGF-1 expression in the myocardial repair process and suggest that synthetic MGF E peptide actions may be mediated via an IGF-1R independent pathway in rat myocardial cells, as suggested by our in vitro experiments. © 2009 The Feinstein Institute for Medical Research.

Cite

CITATION STYLE

APA

Stavropoulou, A., Halapas, A., Sourla, A., Philippou, A., Papageorgiou, E., Papalois, A., & Koutsilieris, M. (2009). IGF-1 expression in infarcted myocardium and MGF E peptide actions in rat cardiomyocytes in vitro. Molecular Medicine, 15(5–6), 127–135. https://doi.org/10.2119/molmed.2009.00012

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free